386 tongue tie (ankyLogLoSSia) Once the tongue can be protruded beyond the lower inci-
A mobile tongue helps not only in speech but also in main- sors it should not cause speech defects.
taining orodental hygiene. It cleans the debris and prevents Treatment: Thick significant tongue tie needs transverse
formation of dental plaques. surgical release with vertical closure. Thin mucosal fold is
True tongue tie, which produces symptoms, is not common. simply incised.
Section 4 w oral cavity and Salivary glands clinical highlights
1. fordyce’s spots: They represent normal variants of ectopic sebaceous glands. Fordyce’s spot present as granules in
oral cavity.
2. precancerous lesions: Oral lesions having malignant potential are erythroplakia (erythroplasia), leukoplakia, lichen
planus and submucous fibrosis.
3. Wickham’s striae: It is a feature of lichen planus.
4. Leukemia: Oral findings include pale mucous membrane, gingival hypertrophy and petechial hemorrhages.
5. hand, foot and mouth disease: It is caused by Coxsackie A virus.
6. hiV: Oral manifestations include oral candidiasis, hairy leukoplakia and recurrent aphthous ulcers.
7. taste buds: They are in highest number (250) in circumvallate papillae and least (1–18) in fungiform papillae. There are
practically no buds in filiform papillae. Foliate papillae have second highest number (100) of taste buds.
further reading
1. Management submucous fibrosis of oral cavity. Reader’s Forum-21. Indian J Otolaryngol Head Neck Surg. 2000;52:328.
2. Purohit JP, Sharma VK, Singh PN. Leukoplakia: correlative study of clinical picture and cytohistopathology. Indian J Otolaryngol Head
Neck Surg. 2000;52:33-6.
3. Raina C, Raizada RM, Chaturvedi VN, et al. Clinical profile and serum beta-carotene levels in oral submucous fibrosis. Indian J Otolaryngol
Head Neck Surg. 2005;57:191-5.
4. Ramadass T, Manokaran G, Pushpala SM, et al. Oral submucous fibrosis-new dimensions in surgery. Indian J Otolaryngol Head Neck
Surg. 2005;57:99-102.
5. Sandu K, Makharia SM. Unusual Experience in OSMF. Indian J Otolaryngol Head Neck Surg. 2004;56:65-6.
6. Talsania JR, Shah UB, Shah AI, et al. Use of diode laser in oral submucous fibrosis with trismus: prospective clinical study. Indian J
Otolaryngol Head Neck Surg. 2009;61:22-5.
7. How do you treat recurrent Aphthous stomatitis? Reader’s Forum-17. Indian J Otolaryngol Head Neck Surg. 2000;52:201-2.
36 Disorders of Salivary Glands
We need to have three things: the heart to feel, the brain to conceive, the hand to work. Make yourself a dynamo. If you are pure,
if you are strong, you, one man, are equal to the whole world.
— Swami Vivekananda
points of focus neoplaSmS of SaliVary glandS
¯ hiStogeneSiS of neoplaSmS
¯ introduction ¯ pleomorphic adenoma
¯ Warthin’S tumor
inflammatory diSorderS ¯ oncocytoma
¯ mumpS ¯ hemangioma
¯ acute SuppuratiVe SialadenitiS ¯ lymphangiomaS
¯ parotid abSceSS ¯ mucoepidermoid carcinoma
¯ neonatal SuppuratiVe parotitiS ¯ adenoid cyStic carcinoma
¯ recurrent parotitiS of childhood ¯ acinic cell carcinoma
¯ chronic SialadenitiS ¯ SquamouS cell carcinoma
¯ malignant mixed tumor
Benign lymphoepithelial lesion ¯ adenocarcinoma
Kuttner’s tumor ¯ lymphoepithelial carcinoma
¯ tuberculouS mycobacterial diSeaSe
¯ nontuberculouS mycobacterial diSeaSe xeroStomia
¯ actinomycoSiS
¯ cat Scratch diSeaSe ¯ SjÖgren’S Syndrome
¯ toxoplaSmoSiS ¯ diffuSe infiltratiVe lymphocytoSiS Syndrome
¯ hiV-aSSociated SaliVary gland diSeaSe ¯ frey’S Syndrome
¯ clinical highlightS
obStructiVe diSorderS
¯ SialolithiaSiS
introduction Congenital disorders, which include aplasia/agenesis,
Salivary gland disorders can be broadly divided into following ductal atresia, fistula and ectopic salivary tissue, are rare.
categories:
Congenital inflammatory diSorderS
Inflammatory
Obstruction and trauma mumpS
Neoplasms Mumps is derived from Danish word “mompen” that means
Degenerative conditions mumbling like an old man, which occurs in mumps due to
pain and trismus.
388 etiology Dietary modifications to minimize glandular secretory
activity.
Section 4 w oral cavity and Salivary glands Mumps is an acute viral parotitis, which is caused by the para- Fever usually subsides before the resolution of glandular
myxovirus (RNA virus). Other viruses, which can cause acute
viral parotitis, are: coxsackie viruses A and B, enteric cytopathic edema, which may take several weeks.
human orphan virus, cytomegalovirus and lymphocytic chorio-
meningitis virus. complications
Orchitis, aseptic meningitis, pancreatitis, nephritis and senso-
epidemiology rineural hearing loss.
It is the most common cause of nonsuppurative acute sial- prevention
adenitis. It mostly affects children. Subcutaneous injection of vaccination (live attenuated
Jerry Lynn vaccine), usually in combination with measles
Mumps is highly contagious. and rubella vaccines is given after 12 months of age. The
The peak incidence occurs in the spring in temperate antibodies produced by vaccine, persist for at least 5 years.
The vaccine is contraindicated in pregnancy, immunocom-
climates (little variation in tropics). promised states and allergies to neomycin.
The paramyxovirus is endemic in the community. It is
acute SuppuratiVe SialadenitiS
disseminated by means of airborne droplets from salivary, The parotid is most commonly involved salivary gland. The
nasal and urinary secretions. parotid gland’s serous saliva, unlike mucinous saliva of other
This paramyxovirus enters through the upper respiratory salivary glands, is deficient in lysosomes, IgA antibodies and
tract and then localizes in glandular and central nervous sialic acid, which have antimicrobial properties. The saliva from
system tissue. other glands (submandibular and sublingual glands) contains
It has an incubation period of 2–3 weeks. high molecular weight glycoproteins that competitively inhibit
Viral infection of salivary glands may be locally asymptom- bacterial attachment to the epithelial cells of the salivary ducts.
atic. The transmission from blood to saliva occurs without
localizing signs in many systemic viral infections such as
rabies, hepatitis, influenza and poliomyelitis.
clinical features predisposing factors
Viral prodome: Low-grade fever, headache, myalgia, Age: It usually affects 50 and 60 years old people (equal
anorexia, arthralgia and malaise just before parotid swelling. incidence among men and women).
Mumps is characterized by localized pain, which is exacer- Debilitating conditions: Malignant lesion and pre-existing
bated by chewing. infection.
Parotid gland swelling is tense and firm. Postoperative period: Major abdominal and hip repair surgery.
Painful swelling of the gland causes displacement of the
It occurs within the first two postoperative weeks.
pinna, otalgia, trismus and dysphagia. Local: Stenosis and sialolithiasis.
There is bilateral parotid gland swelling in 75% of cases Systemic diseases: Diabetes mellitus, hypothyroidism, renal
but submandibular gland might be affected in rare cases. failure and Sjögren’s syndrome.
Usually one side parotid will swell first followed by enlarge- Dehydration or significant hemorrhage: The retrograde
ment of the other gland in 1–5 days.
The overlying parotid skin is stretched with a glazed appear- bacterial contamination of the salivary ducts from the
ance, but there is usually no erythema or warmth. oral cavity occurs due to the stasis of salivary flow. It is
secondary to dehydration or significant hemorrhage.
investigation Medications.
Viral serology: Complement fixing soluble (S) antibodies
causative microorganisms
against the nucleoprotein core of the virus is associated with Penicillin resistant Staphylococcus aureus in hospitalized
active infection and their levels peak at 10 days to 2 weeks
and disappear within 8–9 months. A fourfold increase in patients.
antibody titer is diagnostic for acute infection. Complement Streptococcus pyogenes, Streptococcus viridans, Streptococcus
fixing viral (V) antibodies against outer surface hemag-
glutinin appear later than S antibodies and persist at low pneumoniae and Haemophilus influenzae (community-
levels for many years. acquired cases).
A leukocyte count may show leukopenia. Anaerobic bacteria: Peptostreptococcus, bacteroides species
There is an elevation in the serum salivary type amylase. and fusobacterium.
treatment clinical features
Supportive measures include It usually presents with rapid onset of pain and swelling over
Bed rest
Oral hygiene the affected salivary gland, fever, chills and malaise.
Hydration Dehydration with dry mucous membranes and local tender-
ness, warmth and induration.
Bimanual palpation results in suppurative discharge from
the duct orifice.
investigations parotid abSceSS 389
Multiple small abscesses may coalesce and form large
Leukocytosis with neutrophilia and normal serum amylase.
Computed tomography (CT) or ultrasound (US) is indicated abscess in an advanced case of suppurative parotitis (Fig. 1).
to look for abscess formation if patient does not respond An US examination of the swelling will reveal the abscess. the
to medical treatment. usual fluctuation may not be elicited due to the dense fibrous
Cultures of purulent drainage from the duct orifice. capsule (derived from investing layer of deep cervical fascia)
Percutaneous needle aspiration limits the amount of of the parotid gland.
contamination.
Figures 2A and B show contrast CT scan left parotid abscess.
differential diagnoses
treatment
Usually the diagnosis is apparent. Differential diagnoses Incision and drainage: In addition to the treatment of acute
include lymphoma, Bezold’s abscess, cervical adenitis, dental
abscesses presenting as buccal or masseteric space abscesses, parotitis abscess needs incision and drainage. It is done
infected branchial cleft or sebaceous cysts. under the cover of antibiotics. An anterior based facial flap
treatment fig. 1: Left side parotid abscess. 57 year-old-male diabetic ir- chapter 36 w disorders of Salivary glands
It begins with aggressive medical treatment and includes: radiated patient of right side carcinoma tonsil. Patient had painful
Prompt fluid and electrolyte replacement, oral hygiene, swelling that reduced in size with antibiotics and abscess got
localized
reversal of salivary stasis and antimicrobial therapy.
Salivary flow should be stimulated by sialogogues such as
lemon drops and orange juice.
Regular external and bimanual massage, starting from the
distal bed of the gland and working in the direction of duct
drainage helps greatly in drainage.
Analgesics and local heat application alleviate discomfort.
Antimicrobial therapy, which might need change after the
culture results, should be continued for 1 week after resolu-
tion of symptoms. Antibiotics include augmented penicillin
(Beta-lactamase producing bacteria in 75% cases) and
antistaphylococcal penicillin or a first-generation cephalo-
sporin, vancomycin or linezolid (for methicillin-resistant S.
aureus infection) and metronidazole (for anaerobes).
Surgical drainage of a loculated abscess is done if conserva-
tive measures fail.
ab
figs 2a and b: Contrast CT scan left parotid abscess. Coronal images show peripherally en-
hancing hypodense lesion in left parotid gland
Source: Dr Swati Shah, Professor, Radiodiagnosis, GCR Medical College, Ahmedabad
390 is elevated. With blunt dissection and radial incisions in the Exacerbations occur every 3–4 months and last for days
parotid fascia abscess is drained. Radial horizontal incisions to weeks.
Section 4 w oral cavity and Salivary glands prevent injury to the facial nerve branches which run in
same direction. Drain should be placed and the central Sialography: Sialectasis appears as numerous scattered
aspect is left to heal by secondary intention. punctate pools of contrast.
complications Ultrasound: An enlarged gland with multiple small
Suppuration of potential spaces of the face, neck and hypoechoic areas.
mediastinum. MR Sialography: This noninvasive study may be used during
Rupture through the floor of the external auditory canal or acute episodes.
spontaneous drainage through the cheek. Pus must be sent for culture.
Rare complications are osteomyelitis, thrombophlebitis of
treatment
the jugular vein, septicemia, respiratory obstruction and Treatment includes
even death. Adequate hydration
In cases of facial nerve paralysis, underlying malignancy Gland massage
must be ruled out. Local heat
Sialagogues
neonatal SuppuratiVe parotitiS Appropriate intravenous penicillinase-resistant antistaphy-
This uncommon condition mostly affects parotid gland. lococcal antibiotics.
Neonatal suppurative parotitis, common in preterm and male Most cases resolve spontaneously in late adolescence.
neonates, is usually caused by S. aureus (most common),
Escherischia coli, Pseudomonas aeruginosa and group B strepto-
cocci. Infections are either through oral cavity (most common)
or blood borne (usually gram-negative bacteria). Fever,
anorexia, irritability and failure to gain weight are present in
affected child. Erythema of the skin overlying the involved
gland might be observed. The swelling, which is tender, firm or
fluctuant often becomes bilateral. Gram’s stain and culture of
pus from the duct or from fine needle aspiration (FNA) reveals
the causative organisms. Drainage is done when prompt clinical
improvement does not occur with parentral antibiotics or fluc-
tuance of the gland increases.
recurrent parotitiS of childhood fig. 3: Left side acute parotid gland swelling in a
It is the second most common inflammatory salivary gland 10-year-old girl
disease of childhood (8 months to 16 years) after mumps. Boys
are affected more than girls. This disease of unknown etiology
is characterized by periodic episodes of swelling and pain.
Recurrent parotitis of childhood is the second most common
inflammatory salivary gland disease of childhood (8 months to
16 years) after mumps.
proposed etiologies fig. 4: Stensen’s duct opening of right side parotid
gland is congested
Congenital ectasia of portions of the secondary ductal
system predisposes children to S. aureus and S. viridans
colonization
Autosomal inheritance
IgG3 and IgA deficiencies
Juvenile onset primary Sjögren’s syndrome
Viruses are Mumps parotitis, Epstein-Barr virus (EBV) and
HIV.
clinical features
Recurrent episodes of acute or subacute unilateral parotid
gland swelling (Figs 3 and 4) along with fever, malaise and
pain after a meal.
chronic SialadenitiS The submandibular gland is the more commonly involved 391
Salivary stasis, caused by salivary duct obstruction, predisposes gland after systemic tuberculous infection.
to episodes of infection and inflammation. Parotid is the most chapter 36 w disorders of Salivary glands
frequently affected salivary gland. clinical features
Constitutional signs: They include fever and night sweats.
inciting factors
They include sialolithiasis, stricture duct, extrinsic compression Weight loss might be absent.
by tumor, stenosis secondary to scar, congenital dilation and Clinically, there are two different forms.
foreign bodies. An acute inflammatory lesion with diffuse glandular edema:
It may be confused with an acute sialadenitis or an abscess.
clinical features A chronic tumorous lesion: It is seen as a discrete slow
Recurrent swelling and tenderness of the affected gland growing mass that mimics a neoplasm.
associated with eating. differential diagnoses
Minimal saliva can be milked from the duct orifice. Differential diagnoses must include the inflammatory and
Usually the condition is preceded by an attack of acute
neoplastic diseases.
suppurative sialadenitis.
investigations
treatment Chest X-ray is usually negative.
Surgical removal of the gland when conservative management CT images show three patterns:
fails to control symptoms.
Involved lymph nodes are seen as nonspecific homog-
complications enous enhancement.
They include a benign lymphoepithelial lesion, Kuttner’s tumor
and ductal carcinoma. A nodal mass is seen with central lucency and thick rims
of enhancement and minimally effaced fascial planes.
benign lymphoepithelial lesion
Women in the fifth to sixth decade of life are more Fibrocalcified nodes are seen in patients previously
treated for tuberculosis.
commonly affected.
An asymptomatic mass associated with Sjögren’s syndrome Mantoux test: Purified protein derivative skin test should
be positive.
is also termed as Mikulicz’s disease.
FNA cytology and follow-up are important because there Fine needle aspiration cytology: Characteristic cytologic
features include granulomatous inflammation and epithe-
are chances of development of malignancy. lioid histiocytes.
Kuttner’s tumor Culture and acid fast smears of aspiration material.
It occurs exclusively in the submandibular gland.
Middle-aged adults present with painless mass. treatment
There are chances of developing malignancies, so close Anti-Koch therapy: Multiple drug therapy.
Complete surgical excision: In cases in which the diagnosis
follow-up is needed.
is uncertain or the lesion is resistant to medical therapy.
tuberculouS mycobacterial diSeaSe Complete surgical excision is both diagnostic and curative.
the most common manifestation of Mycobacterium tuberculosis nontuberculouS mycobacterial
infection in the head and neck is cervical lymphadenopathy. diSeaSe
Older children and adults are affected more.
More than 92% of mycobacterial cervicofacial infections in children
routes of infections younger than 5 years of age are a result of nontuberculous
Primary salivary tuberculosis is an uncommon entity. mycobacterial (NTM) disease.
Primary infection evolves from a focus in the tonsils or
causative organisms
gingival sulcus ascending to the glands by way of their Mycobacterium kansasii, Mycobacterium scrofulaceum and
ducts. This may then spread to the cervical nodes through Mycobacterium avium intracellulare.
the lymphatic drainage. This most frequently affects the
parotid gland. portal of entry
Secondary infection of the salivary glands occurs by way of It is believed to be through the mouth. Tonsils have been impli-
hematogenous or lymphatic spread from the lungs. cated in particular.
clinical features
Rapidly enlarging and persistent neck mass that fails to
respond to antibiotic therapy in a pediatric patient.
392 The skin becomes adherent to the surrounding tissues and Anaerobic cultures are obtained for species identification
develops a characteristic violaceous discoloration. and to confirm the diagnosis. The recovery rate in culture
Section 4 w oral cavity and Salivary glands is < 50%.
The infection might progress to fluctuation and the devel-
opment of a draining sinus. Smears and stains for sulfur granules and the organisms:
Needle aspiration of the mass or a fistula swab. Sulfur
Associated cervical lymphadenopathy is more commonly granules have also been described for nocardiosis.
unilateral and located in the high jugular nodes or preau-
ricular areas. Biopsy specimens show firm fibrous encasement of multi-
loculated abscesses containing whitish yellow purulent
investigations discharge.
CT images shows asymmetric cervical lymphadenopathy
treatment
with contiguous low density, necrotic, ring enhancing Penicillin 6 weeks parenteral course followed by an addi-
masses involving the subcutaneous fat and skin.
Inflammatory stranding of the subcutaneous fat charac- tional 6 months of oral course completely eradicates the
teristic of bacterial inflammation is minimal or absent. organism.
NTM-specific antigens have been developed and are Other acceptable alternatives include clindamycin, doxy-
reported to be extremely successful for diagnosis. cycline, or erythromycin.
Polymerase chain reaction techniques to detect mycobacte- Surgical excision is necessary to remove extensive fibrosis
rial RNA in tissue and gastric aspirates. and sinus tracts, when antibiotics fail. It also helps in diag-
Traditional culture of NTM might take up to 6 weeks and is nosis.
frequently negative.
prognosis
treatment Prognosis is generally favorable. Cure rates approach 90%
Medical treatment consists of prolonged courses of clar- despite a delayed diagnosis in most instances.
ithromycin. cat Scratch diSeaSe
Complete surgical excision of the involved salivary gland Cat scratch disease is a granulomatous lymphadenitis. It results
from cutaneous inoculation caused by scratch trauma from a
and nodes is the treatment of choice. domestic cat.
actinomycoSiS causative organism
The most common clinical infection is cervicofacial (55%). Bartonella henselae, Gram-negative bacilli.
Isolated parotid involvement can occur by means of either
retrograde ductal migration or of direct spread of an invasive The reservoir for B. henselae is kittens. The major vector for
cervicofacial infection. cats is the cat flea.
causative organism clinical features
Actinomycosis species is a Gram-positive, anaerobic, non- acid- A papule or pustule at a scratch or bite site followed in 1–2
fast bacillus. They are normal commensal in the tonsils and
carious teeth. Actinomyces israelii is the most common. Others weeks by the development of lymphadenopathy in the
include Actinomyces bovis and Actinomyces naeslundii. region of inoculation.
Erythema and fluctuance of the involved nodes with spon-
predisposing factors taneous suppuration occur in 10–30% of patients.
Poor oral hygiene, trauma to the mucosa, diabetes, immune Fever and mild systemic symptoms occur in about one-third
suppression, long-term steroid use and malnutrition. of patients.
Preauricular lymphadenopathy might be confused with a
clinical features parotid neoplasm.
Painless, indurated enlargement of the involved gland: It
diagnosis
might mimic a neoplasm. Antibodies to B. henselae
Multiple draining cutaneous fistulas: It is quite common. A
Indirect fluorescent antibody
chronic purulent drainage might occur with granulomatous Enzyme immunoassay
involvement and spread to adjacent tissue. The periphery Polymerase chain reaction: Bartonella polymerase chain
of the lesion is densely fibrotic and avascular. reaction hybridization assay with an aspirate or biopsy
A history of recent dental disease and manipulation is specimen.
common. Histological examination with Warthin Starry silver staining:
Lymph node shows reticular cell hyperplasia, granuloma
diagnosis formation and widening of arteriolar walls. In more
CT scans typically demonstrate obliteration of the normal advanced stages, stellate areas of necrosis coalesce to form
multiple microabscesses.
tissue planes and extensive soft tissue destruction.
Culture: Bartonella is a slow growing organism and culture MRI reveals homogenous masses of intermediate signal 393
requires a 6 weeks incubation period. intensity on proton density and T2-weighted images.
toxoplaSmoSiS Medical treatment consists of zidovudine, maintenance of
Toxoplasmosis is an uncommon disease. good oral hygiene and the use of sialogogues.
Excision biopsy: Controversial.
causative organism Sialadenitis: Mumps is the most common parotid viral infection.
Toxoplasma gondii: The usual host for this organism is the Less common viral infections are cytomegalovirus, coxsackie
domestic cat. and Epstein-Barr viruses. Bacterial sialadenitis is usually
caused by coagulase positive S. aureus. S. pneumoniae, E.
coli, H. influenzae and oral anaerobe infections may also occur.
clinical features obStructiVe diSorderS chapter 36 w disorders of Salivary glands
Both disseminated and lymphadenopathic forms of the
diseases have been described. SialolithiaSiS
Parotid gland disease might involve singular or multiple The formation of stones in the salivary ductal system is called
sialolithiasis.
intraparotid or periparotid lymph nodes.
Disseminated form: Immunocompromised individuals are etiology
Exact etiology is uncertain. Salivary stasis and ductal inflamma-
most at risk for the disseminated form. The features include tion and injury are important contributing factors.
myalgia, lethargy and anorexia combined with hepato-
splenomegaly, pericarditis and myocarditis. Eighty to ninety percent of calculi develop in Wharton’s duct
Lymphadenopathic form: It occurs commonly. Most patients of submandibular gland. Stensen’s duct of parotid constitutes
present with isolated cervical lymphadenopathy. 10–20% and sublingual duct only 1%. The reasons are the
following:
biopsy Wharton’s duct is longer and has a larger caliber. It is angu-
Definitive diagnosis can only rarely be provided by isolation
of the organism. The characteristic histopathologic findings in lated against gravity as it courses around the mylohyoid
affected lymph nodes include following: muscle.
The lymph node architecture is preserved. Submandibular secretions are more viscous and have a
The hyperplastic follicles and germinal centers show abun- higher calcium and phosphorus concentration.
Parotid stones are mostly located at the hilum or paren-
dant mitoses and necrotic nuclear debris. chyma, while in the submandibular gland, they tend to develop
Epithelioid cells, with abundant, pale eosinophilic cyto- in the duct. Elderly people are more affected than children. Most
of the patients are male.
plasm. They occur singly or in groups and are found in
cortical and paracortical zones and sinuses.
Confirmation of a presumptive histological diagnosis is made
by acute and convalescent serologic testing.
treatment composition
Chemotherapy (combined administration of pyrimethamine They are composed mainly of calcium phosphate and carbonate
and trisulfapyrimidines) is generally reserved for obviously in combination with an organic matrix of glycolproteins and
progressive infections or those involving pregnant or immu- mucopolysaccharides and small amounts of other salts such
nocompromised individuals. as magnesium, potassium and ammonium.
hiV clinical features
HIV lesions of salivary glands include Kaposi’s sarcoma, Recurrent episodes of postprandial salivary colic pain and
lymphoma and lymphoproliferative and cystic enlargement of
the major salivary glands with accompanying salivary dysfunc- swelling.
tion. Past history of recurrent attacks of acute suppurative sial-
hiV-associated Salivary gland disease adenitis might be present.
It refers to diffuse enlargement of the salivary glands due to Bimanual palpation reveals the presence of a stone in most
HIV. Parotid gland is the most commonly affected. Salivary
secretions contain low concentrations of HIV. cases.
Parotid stones might be seen just at the orifice of Stensen’s
Clinical features: Patients usually presents with gradual,
nontender enlargement of one or more of the salivary glands. duct or along the course of the duct.
Decreased salivary gland function results in xerostomia and
sicca symptoms. investigations
Plain radiographs (intraoral or occlusal views) identify radi-
CT demonstrates multiple cysts that appear as low attenu-
ation, thin walled masses and diffuse lymphadenopathy. opaque stones but in the submandibular gland 80% of
stones are radiolucent.
Ultrasound: It detects 90% of stones if they are > 2 mm.
CT scanning with fine cuts is very accurate at detecting
salivary stones.
394 Digital subtraction sialography, which lessens the interfer- the salivary gland tumors arise in the parotid gland (Fig. 6). The
ence of surrounding bony structures, can detect 95–100% chances of a tumor being benign are more in major salivary
Section 4 w oral cavity and Salivary glands of radiolucent stones. glands (80% of parotid and 50–60% of submandibular) while
less in minor salivary glands (25%). Therefore, majority of the
MR sialography of the submandibular duct with evoked minor salivary glands tumors are malignant. The sign and symp-
salivation is superior to US and has accuracy similar to digital toms of malignancy are: rapid growth, restricted mobility, fixity
subtraction sialography. of overlying skin, pain and facial nerve involvement.
treatment The tumors of salivary glands are either of epithelial or
Nonsurgical management: It consists of the use of: mesenchymal origin (Table 1). Pleomorphic adenoma is the
most common salivary gland tumor and the number two is
Sialogogues mucoepidermoid carcinoma. Other tumors in series of common
Local heat frequency are: adenoid cystic carcinoma, adenocarcinoma,
Hydration malignant mixed tumor and Warthin’s tumor (second most
Massaging of the involved gland common benign tumor). The pleomorphic adenoma of the
Antibiotic coverage is started in cases of infection. parotid gland needs surgical excision that provides both defini-
Manually milking out: Submandibular stones nearer the tive diagnosis and adequate treatment. Management of other
types of salivary neoplasms is challenging because of their
duct orifice may be manually milked out through the relative infrequency and variable biologic behavior.
duct opening (Figs 5A to C).
Surgical management: It consists of: hiStogeneSiS of neoplaSmS
Incision of duct: Submandibular stones, which are no The two main theories of tumorigenesis, proposed for salivary
more than 2 cm from the duct orifice, may be either gland neoplasms, are multicellular and bicellular reserve cell
manually milked out through the duct opening or the theories.
duct is incised directly over the stone. There is no need
for closure of Wharton’s duct after the procedure.
Sialadenectomy: Submandibular stones located more
proximal and near gland will require sialadenectomy,
which may be performed either through transcervical
or transoral approach. Parotid stones are more difficult
to manage because of the anatomy of Stensen’s duct.
Recent advances: Use of various combination of baskets,
graspers and intracorporeal lithotripsy have been employed
to treat sialolithiasis in both the parotid and submandibular
glands.
Extracorporeal shock wave lithotripsy reduces stones
to small fragments, which are then flushed out of the
duct with spontaneous salivation or the use of a secre-
tagogue.
Sialoendoscopy: Rigid endoscopes are used to visualize
and remove salivary duct stones.
neoplaSmS of SaliVary glandS fig. 6: Swelling of the parotid gland
Salivary gland tumors, majority of which are benign, constitute table 1 Tumors of salivary glands
just 3–4% of all head and neck neoplasms. Seventy percent of
Benign Malignant
ab
Epithelial (Adenomas) Epithelial
c
• Pleomorphic adenoma • Mucoepidermoid
figs 5a to c: Wharton’s duct calculus. This patient had right • Adenolymphoma carcinoma
submandibular abscess. (A) Right side Wharton’s duct calculus
coming out from its opening; (B) Appearance of Wharton’s duct (Warthin’s tumor) • Adenoid cystic carcinoma
opening (too much dilated) after the milking out of calculus. The • Oncocytoma (cylindroma)
submandibular abscess drained through this opening; (C) Gross
appearance and measurement of the removed Wharton’s duct • Monomorphic adenoma • Acinic cell carcinoma
calculus
Mesenchymal • Adenocarcinoma
• Vascular: Hemangioma • Malignant mixed tumor
• Lymphatic: • Squamous cell carcinoma
lymphangioma • Undifferentiated carcinoma
• lipoma Mesenchymal
• Neurofibroma • lymphoma
• Benign cyst • Sarcoma
1. Multicellular cell theory: Each neoplasm is thought to origi- and nitrosamines (rubber workers) and use of kerosene as 395
nate from a distinctive cell type. All differentiated salivary cooking fuel have been reported associated with increase
cell types retain the ability to undergo mitosis and regenera- the risk of malignancy in salivary glands. chapter 36 w disorders of Salivary glands
tion. 5. Hormonalfactors:Women with a history of early menarche
a. Warthin’s and oncocytic tumors arise from striated and nulliparity were found to have increased risk of devel-
ductal cells, oping cancer of salivary glands.
b. Acinic cell tumors arise from acinar cells, and 6. Hair dye and alcohol intake in women have been
c. Mixed tumors arise from intercalated duct and myoepi- reported to increase the risk of developing cancer of
thelial cells. salivary glands.
7. Dietary factors: Vegetables preserved in salt were found
2. Bicellular reserve cell theory: According to this theory, various associated with twofold risk of salivary malignancy.
types of salivary neoplasms originate from the basal cells 8. Genetic factors: Genetic aberrations, which are found
(pluripotential cell populations) of either the excretory or the associated with the salivary gland neoplasia, include
intercalated duct, which act as a reserve cell with the potential allelic loss and point mutation, structural rearrangement
for differentiation into a variety of epithelial cells. Hence, all the of chromosomal units (most commonly translocations),
heterogeneity salivary tumors are thought to arise from one of the monosomy and the presence of polysomy.
these two cells. Some molecular evidence supports this reserve – Allelic loss: Loss at 12q in pleomorphic adenomas
cell theory.
a. Adenomatoid tumors, including pleomorphic adenoma and multiple losses at 9p, 3p and 17p in carcinoma
and oncocytic tumors arise from reserve cell of interca- ex-pleomorphic adenoma have been reported. Loss
lated duct. of heterozygosity occurs at 8q, 12q and 17p in carci-
b. Epidermoid tumors, such as squamous cell carcinoma noma expleomorphic adenoma (17p in high disease
and mucoepidermoid carcinomas arise from the reserve stage and increased proliferative rate).
cell of the excretory duct. – Monosomy and polysomy: Monosomy (absence of
one chromosome) of chromosome 17 and polysomy
etiology (an extra chromosome) of chromosomes 3 and 17 in
The exact etiology remains unknown but certain environmental salivary gland tumors are higher in adenoid cystic
factors (such as radiation, viruses, diet and certain occupational carcinoma compared with pleomorphic adenoma.
exposures) and specific genetic abnormalities may increase the – Structural rearrangement: Cytogenetically, mono-
risk of developing tumors (Box 1). Some patients of salivary clonal and high frequency of tumor specific chromo-
gland cancer were found to have past history of skin cancer. some bands abnormalities 3p21, 8q12 and 12q14-15
are seen in pleomorphic adenomas of the salivary
box 1: Factors associated with high risk of primary salivary glands. Ectopic expression of the PLAG1 gene occurs
malignancy in ple morphic adenomas with 8q12 aberrations.
• Radiation exposure prophylaxis
• Full mouth dental X-ray The polyunsaturated fatty acids, dark yellow vegetables (carrots
• Skin cancer and sweet potatoes), live stock liver and vitamins A and C have
• Rubber industry been found to offer some protection.
• Nickel compound/alloy
• Hair dye pleomorphic adenoma
• Silica dust This most common benign slow growing tumor of salivary
• Kerosene cooking fuels
• Vegetables preserved in salt. glands, usually arise from the tail of parotid (Fig. 7) and
submandibular glands. It can also arise from minor salivary
1. Radiation: Exposure to ionizing radiation (diagnostic, glands and deep lobe of the parotid, which presents as a
therapeutic, accidental and atomic explosions) may parapharyngeal tumor in the oropharynx (Figs 8 and 9).
increase the risk of developing both benign and malig- The tumor may be quite large at first presentation. It is
nant salivary gland tumors. Risk was higher for malig- usually seen in the third or fourth decade and has propen-
nant tumors especially mucoepidermoid carcinoma. sity for females.
Warthin’s tumor showed the highest dose-response Figures 10A and B show CT scan of pleomorphic adenoma
related risk. The risk of salivary gland neoplasia was not of superficial lobe of right parotid gland with peripheral
found influenced by duration of cellular telephone use. enhancement and well-defined margins.
These “mixed tumors” have both epithelial and mesen-
2. Viral: Epstein-Barr virus has been found associated chymal elements in variable amount. The stroma may be
with lymphoepithelial carcinoma in the Asian popula- mucoid, fibroid, vascular, myxochondroid or chondroid.
tion but there is no evidence of its causal role in other This encapsulated tumor sends pseudopods into the
primary benign and malignant neoplasms of salivary surrounding glands, therefore it is essential that surgical
glands. Other viruses including human papillomavirus, excision of the tumor should include surrounding normal
human herpesvirus 8 and cytomegalovirus do not gland tissue. These pseudopods may be left behind if the
have any etiologic role. tumor is simply “shelled out”. Superficial parotidectomy is
done for superficial parotid tumor.
3. Smoking: Warthin’s tumor is found associated with ciga-
rette smoking.
4. Occupational factors: Exposure to silica dust, nickel alloys
396 Warthin’S tumor or adenolymphoma
(papillary cyStadenoma
lymphomatoSum)
Warthin’s tumor is commonly seen between fifth and
seventh decade with male preponderance (5:1).
The most common site is the tail of the parotid and is bilat-
eral in 10% cases. They may be multiple.
It is a rounded encapsulated tumor, which may be at times
cystic with mucoid or brownish fluid.
Histopathology shows its epithelial and lymphoid elements.
Usually superficial parotidectomy is performed. However,
they can be enucleated without danger of recurrence.
Section 4 w oral cavity and Salivary glands fig. 7: Swelling of the tail of parotid gland oncocytoma
It comprises less than 1% of all salivary gland tumor and
usually does not grow more than 5 cm in size.
This oxyphil adenoma arises from acidophilic cells (onco-
cytes). It is mostly seen in the superficial parotid lobe of the
elderly people.
Oncocytoma shows increased uptake of technetium-99. It
may be malignant, benign or cystic in nature.
Treatment is superficial parotidectomy.
hemangiomaS
Hemangiomas are the most common benign parotid tumors
in children and predominantly affect females.
Congenital hemangioma grows rapidly in the neonatal
period and then involutes spontaneously. Cutaneous
hemangioma coexists in 50% of the cases.
Characteristically, they are soft and painless and increase
in size with crying or straining. The overlying skin shows
bluish discoloration.
Treatment is surgical excision if they do not regress.
fig. 8: Parotid tumor axial view. Tumor extending into para- lymphangiomaS
pharyngeal space posterior to stylomandibular ligament
These less common tumors feel soft and cystic and involve
parotid and submandibular glands.
They do not regress in size spontaneously and need surgical
excision.
fig. 9: Parotid tumor coronal view. Dumb-bell parotid tumor mucoepidermoid carcinoma
extending into parapharyngeal space anterior to stylomandibular This slow growing malignant tumor of parotid can metas-
ligament through the stylomandibular membrane between the
stylomandibular ligament and mandible tasize and involve facial nerve. Mucoepidermoid tumors of
minor salivary glands are more aggressive while in major
salivary glands they behave like pleomorphic adenoma.
The mucoepidermoid tumor has both the areas of mucin
producing cells as well as squamous cells.
The tumors have been classified as low grade and high
grade. The tumors, which have greater epidermoid element,
are more malignant.
Low grade tumors are more common in children. They
have good prognosis and 90%, 5 years survival rates.
High grade tumors are more aggressive. They have poor
prognosis and 30%, 5 years survival rate.
Staging
Tumor, nodes and metastases (TNM) classification of major
salivary gland malignancy is shown in Table 2.
397
ab chapter 36 w disorders of Salivary glands
figs 10a and b: CT scan coronal (A) and axial (B) sections. Pleomorphic adenoma right parotid lesion in superficial lobe with pe-
ripheral enhancement and well-defined margins
Source: Dr Swati Shah, Professor, Radiodiagnosis, GCRI Medical College, Ahmedabad
treatment adenoid cyStic carcinoma
Low grade parotid tumors are managed by superficial or (cylindroma)
This is a slow growing tumor, which infiltrates widely into
total parotidectomy. Surgery depends upon the location
and extent of the tumor (Table 2). Facial nerve is preserved. the tissue planes and muscles.
The aggressive high grade tumors need total parotidectomy It spreads through perineural spaces and lymphatics and
and facial nerve is sacrificed if invaded by tumor. Facial
nerve is grafted in same sitting. causes pain and facial nerve palsy.
If needed radical neck dissection is also combined. Distant metastases can occur in lungs, brain and bones.
table 2 American Joint Committee on Cancer (AJCC) Cancer Staging (2002) and UICC TNM classification of malignant
tumors of major salivary glands
tx Primary tumor cannot be assessed
t0 No evidence of primary tumor
t1 Tumor <= 2 cm size
t2 tumor 2–4 cm
t3
t4a tumor more than 4 cm or extraparenchymal extension
t4b
Nx Tumor invades skin, mandible, ear canal, or facial nerve
N0 Tumor invades skull base, pterygoid plates, or encases carotid artery
N1 Regional lymph nodes cannot be assessed
N2a No regional lymph node metastasis
N2b Metastasis in a single ipsilateral lymph node 3 cm or less
N2c Metastasis in single ipsilateral lymph node 3–6 cm
N3 Metastasis in multiple ipsilateral lymph nodes < 6 cm
Mx Metastasis in bilateral or contralateral lymph nodes < 6 cm
M0 Metastasis in lymph node > 6 cm
M1 Distant metastasis cannot be assessed
Stage grouping No distant metastasis
Distant metastasis
Stage I t1 N0 M0
Stage II t2 N0 M0
Stage III t3 N0 M0; t1-3 N1 M0
Stage IVA t4a N0-1 M0; t1-4a N2 M0
Stage IVB t4b N0-3 M0; t1-4b N3 M0
Stage IVC t1-4b N0-3 M1
398 treatment > 4,000 cGy will result in severe and permanent secretory
Treatment is by radical parotidectomy, which includes large hypofunction.
Section 4 w oral cavity and Salivary glands Xerostomia and xero-ophthalmia, the most common
surrounding normal tissue. presentation of Sjogren’s s syndrome, is also called Mikulicz
Radical neck dissection is done if nodal metastases are disease.
present. SjÖgren’S Syndrome
Postoperative radiation is given if the margins of the tumor Sjögren’s syndrome is a chronic autoimmune disorder of the
exocrine glands. The salivary and lacrimal glands are primarily
are not clear. affected. The lymphocytic infiltration results in glandular hypo-
Local recurrences after surgical excision, which may be as function leading to dryness of the mouth and eyes. The disease
might even evolve into a malignant lymphoid process.
late as 10–20 years, are common.
types
acinic cell carcinoma 1. Primary Sjögren’s syndrome: This type of Sjögren’s syndrome
This low grade tumor appears similar to a benign mixed tumor.
It presents as a small, firm, movable and encapsulated tumor. is confined to the exocrine glands.
Bilateral tumors are also seen. Metastases are rare. 2. Secondary Sjögren’s syndrome: Patients have the character-
Treatment is superficial or total parotidectomy. istic signs and symptoms of primary Sjögren’s syndrome
associated with features of other autoimmune disease.
SquamouS cell carcinoma
This rapidly growing painful tumor infiltrates and ulcerates Secondary Sjögren’s syndrome is the triad of: kerato-
through the skin, and metastasizes to neck nodes. conjunctivitis sicca (involvement of lacrimal gland), xerostomia
(involvement of salivary glands and mucous glands of the oral
Treatment is by radical parotidectomy, which includes cavity) and autoimmune connective tissue disorders such as
surrounding part of muscle, mandible, temporal bone and the rheumatoid arthritis.
involved skin. Radical neck is combined if nodal metastases are
present. Postoperative radiotherapy is given. epidemiology
The estimated prevalence of Sjögren’s syndrome is believed
malignant mixed tumor
This tumor can develop in old benign mixed tumor. Rapid to be 1–3%.
growth and appearance of pain in a slow growing benign The disease is most commonly seen in patients during their
tumor indicates malignant change. A“de novo”tumor has much
shorter history. fourth to fifth decade of life.
More than 90% of patients are women.
Treatment is radical parotidectomy.
etiology
adenocarcinoma Etiology is uncertain and is believed to involve genetics,
This highly aggressive tumor mostly arises in minor salivary
glands and sends distant metastases. immune system and environmental exposures.
lymphoepithelial carcinoma or clinical features
undifferentiated carcinoma Predominant clinical presentation: Dryness of the mouth
This rare aggressive painful tumor has a tendency to spread and eyes.
rapidly. It becomes fixed to skin and ulcerates. It causes facial Salivary gland enlargement is most common in the parotid
paralysis and cervical nodal metastasis. Treatment is wide exci-
sion combined with radical neck dissection and postoperative glands and occurs in 25–66% of patients. The bilateral
radiotherapy. enlargement may be recurrent and episodic or chronic
and fixed.
Malignancy of salivary glands: Their presentation may be similar Patients with persistent unilateral or bilateral parotid gland
to benign tumors and can lead to delay in diagnosis. enlargement are at higher risk for the development of
lymphoma.
xeroStomia
oral findings
Xerostomia refers to dryness of mouth resulting from dimin- Xerostomia causes difficulty in chewing, swallowing and
ished or arrested salivary secretion. Xerostomia causes difficulty
in chewing, swallowing and phonation, adherence of food to phonation, adherence of food to the buccal mucosa and
the buccal mucosa and multiple dental caries. multiple dental caries.
Diabetes and cystic fibrosis should be assessed. Intolerance to acidic and spicy foods is a common
Sedatives, antipsychotics, antidepressants, antihistamines complaint.
and diuretics are most often associated with oral dryness.
Salivary gland exposure to therapeutic irradiation
Dry and sticky oral mucosal surfaces. Systemic sialogogues: Pilocarpine (muscarinic cholinergic 399
Absence of pooled saliva in the floor of the mouth. agonist) 5 mg three to four times daily, side effects include
The tongue is typically smooth with fissures and atrophy sweating, flushing and increased urination. chapter 36 w disorders of Salivary glands
of the filiform papillae. Treatment for keratoconjunctivitis: Eye lubricants and eye
Intraoral fungal overgrowth with Candida albicans. patching if corneal ulceration develops.
Expression of scant or cloudy saliva from the salivary ducts.
Systemic corticosteroids or cytotoxic drugs: They are reserved
Objective evaluation of salivary flow rate can be performed for the severe extraglandular complications such as glomer-
with Lashley cups that fit over the opening of Stensen’s ulonephritis or necrotizing vasculitis.
duct and collect saliva.
Sjögren’s syndrome: A positive ANA, RF, SS-a, SS-b and an
eye findings elevated ESR are indicative of Sjögren’s syndrome. Biopsy from
lip confirms the diagnosis and shows atrophy of minor salivary
Most common ocular complaint: Foreign body sensation in glands with an abundance of lymphocytes and histiocytes.
the eye (“gritty” or “sandy” feeling).
diffuSe infiltratiVe lymphocytoSiS Syn-
Chronic irritation and destruction of the corneal and drome
conjunctival epithelium causes keratoconjunctivitis sicca.
The sicca symptom complex clinically mimics Sjögren’s
Dilation of the bulbar conjunctival vessels, pericorneal syndrome. It is characterized by the presence of persistent
injection, irregularity of the corneal image and occasionally circulating CD8 lymphocytosis and visceral CD8 lympho-
enlargement of the lacrimal gland. cytic infiltration (predominantly in the salivary glands and
lungs).
Schirmer’s test: For tear secretion rate assessment.
Staining of damaged corneal and conjunctival epithelia Autoantibodies present in Sjögren’s syndrome are absent in
diffuse infiltrative lymphocytosis syndrome (DILS).
by rose Bengal dye is specific for keratoconjunctivitis sicca.
Findings of needle aspiration and CT or MRI are sufficiently
Systemic manifestations typical to provide a presumptive diagnosis.
Generalized malaise, low grade fever, myalgia and arthralgia, This condition is treated with corticosteroids and immuno-
bronchitis or pneumonia, renal tubular acidosis, vasculitis suppressive therapy.
(Raynaud’s phenomenon and recurrent urticaria-like lesions),
peripheral sensory and motor polyneuropathies. frey’S Syndrome (guStatory
SWeating)
laboratory investigations
Gustatory sweating manifests several months after the
Laboratory investigations show raised erythrocyte sedime- parotid operation. It is characterized by sweating and
ntation rate, positive rheumatoid factor and positive antin- flushing of the preauricular skin during mastication.
uclear antibodies. Biopsy from the lower lip shows evidence
of involvement of minor salivary glands. This condition is the result of aberrant innervation of sweat
Sialography: Sialectasis is seen in 85–97% of patients. glands by parasympathetic secretomotor fibers which were
Testing for autoantibodies to the ribonuclear proteins Ro destined for the parotid. Thus, these postganglionic fibers
from the otic ganglion carried by auriculotemporal nerve,
(SS-A) and La (SS-B) is done by use of enzyme-linked immu- instead of causing salivary secretion cause secretion from
nosorbent assay. the sweat glands.
Biopsy: The biopsy of labial accessory salivary glands is taken
from areas with normal overlying mucosa. The histopa- The placement of a sheet of fascia lata between the skin
thology shows a lymphocytic infiltrate producing a chronic and the underlying fat may prevent secretomotor fibers
focal sialadenitis and multiple focal mononuclear aggre- reaching the sweat glands.
gates that are adjacent to and replace the normal acini.
treatment
treatment
Usually no treatment other than reassurance is required.
The treatment consists of symptomatic therapy and prevention In cases of significant nuisance and social embarrass-
of irreversible damage to the teeth and eyes.
Saliva substitutes and chewing of sugarless gum or candies. ment, the condition is treated by tympanic neurec-
Fluoride: for treating and preventing dental caries. tomy of Jacobson’s nerve, which carries preganglionic
Eradicating fungal overgrowth. parasympathetic secretomotor fibers from the inferior
salivary nucleus through the glossopharyngeal nerve.
400 clinical highlights
Section 4 w oral cavity and Salivary glands 1. complications of mumps: They include unilateral sensorineural hearing loss, thyroiditis, pancreatitis, and orchitis.
2. Sarcoidosis: The clinical features include parotid swelling, facial paralysis, cervical lymphadenopathy, and diabetes
insipidus.
3. Salivary calculi: Eighty percent of salivary calculi are seen in submandibular gland. Twenty percent of submandibular
gland calculi are radiolucent.
4. Nonneoplastic and noninflammatory parotid swellings: The common causes are obesity, hypothyroidism, diabetes
mellitus, and malnutrition.
5. parotid tumor: Most common parotid tumor in children is lymphoma. Parotid gland is the most common site of pleomorphic
adenoma.
6. hemangioma: It is present in neonates with an isolated unilateral parotid swelling with bluish overlying skin. Swelling
increases when child cries.
7. adenoid cystic carcinoma: It is the most common malignant tumor of the submandibular salivary gland. Adenoid cystic
carcinoma has a tendency for perineural invasion.
8. acinous cell carcinoma: Among the malignancies of parotid gland, this has the best prognosis.
9. Superficial parotidectomy: This surgical treatment is adequate in cases of oncocytoma, pleomorphic adenoma, basal
cell adenoma, and acinic cell carcinoma of parotid gland. Because of the section of greater auricular nerve, superficial
parotidectomy is followed by anesthesia of the lower part of pinna.
10. xerostomia: Some of the causes are antihistamines, uremia, Sjögren’s syndrome, and mouth breathing.
11. Sjogren’s syndrome: This autoimmune disease associated with collagen disorder is predominantly seen in women
(9:1) between the ages of 40 and 60 years. Dryness of the eyes and dry mouth are the most common features. Parotid
enlargement, which may be chronic or relapsing, develops in one-third of patients. Three to ten percent patients develop
lymphoma.
12. mikulicz disease: Treatment of choice is steroid therapy.
13. frey’s syndrome (gustatory sweating): This is the flushing and sweating of skin of parotid region during eating in
parotidectomy patients. Parasympathetic postganglionic secretomotor fibers supplying the parotid gland are misdirected
and innervate (to postganglionic sympathetic fibers supplying the sweat glands) skin of the parotid area. Sectioning of
the Jacobson’s nerve (tympanic branch of glossopharyngeal nerve carrying preganglionic secretomotor fibers for parotid
gland) on the promontory of middle ear (tympanic neurectomy) alleviate the symptoms.
further reading
1. Arora V, Samdhani S, Bapna AS. Stony Wharton’s Duct. Indian J Otolaryngol Head Neck Surg. 2001;53:242-3.
2. Chandrakala SR, Crasta JA, Shariff S. Cytodiagnosis of submandibular sialadenitis with crystalloids mimicking metastasis. Indian J Oto-
laryngol Head Neck Surg. 2003;55:275-7.
3. Dubey A, Murthy JG, Banerjee PK. Actinomycosis of the parotid gland. Indian J Otolaryngol Head Neck Surg. 2004;56:306- 8.
4. Gupta SC, Singla A, Singh M, et al. Effects of radiotherapy on parotid salivary sialochemistry in head and neck cancer
patients. Indian J Otolaryngol Head Neck Surg. 2009;61:286-90.
5. Kamath MP, Bhojwani KM, Jayalaxmi Bhat M, et al. Pleomorphic adenoma. Indian J Otolaryngol Head Neck Surg. 2005;Special issue-
II:499-500.
6. Mehta B, Tiwari RS. Submandibular sialolithiasis: Unusual case with five stones in one duct. Indian J Otolaryngol Head Neck Surg.
2005;Special issue-II:492-3.
7. Nagarkar NM, Bansal S, Dass A, et al. Salivary gland tumors—our experience. Indian J Otolaryngol Head Neck Surg. 2004;56:31-4.
8. Sengupta S, Roy A, Mallick MG, et al. FNAC of salivary glands. Indian J Otolaryngol Head Neck Surg. 2002;54:184-8.
9. Shenoy A, Ravi S, Nanjundappa, et al. Tumours of the parotid- changing trends in treatment philosophy. Indian J Otolaryngol Head Neck
Surg. 2005;Special Issue-II:366-8.
10. Sohal BS, Verma SK, Gill GPS, et al. Pleomorphic adenoma of submandibular gland. Indian J Otolaryngol Head Neck Surg. 2004;56:216-7.
11. Tuli BS, Gupta V, Singh H, et al. Primary tuberculosis of parotid gland. Indian J Otolaryngol Head Neck Surg. 2005;57:82-3.
12. In a case of Submandibular Salivary Calculus, do you remove intra orally? When do you excise Submandibular Salivary Gland in such cases
where obstruction is due to calculus? Any specific technique you follow in intra oral removal? Reader’s Forum. Indian J Otolaryngol Head
Neck Surg. 2005;57:170-2.
37 Neoplasms of the Oral Cavity
Go, all of you, wherever the people are in distress, and mitigate their sufferings. At the most, you may die in the attempt–what of that?
How many like you are being born and dying like worms every day? What difference does that make to the world at large? Die you must,
but have a great ideal to die for and it is better to die with a great ideal in life.
— Swami Vivekananda
Points of focus Clinical Evaluation and Investigations
Staging
¯ introduction Histopathology
benign tumorS of oral caVity Treatment
¯ PaPilloma Prognosis
¯ PleomorPhic adenoma ¯ carcinoma liPS
¯ hemangioma Clinical Features
¯ lymPhangioma Treatment
¯ granular cell tumor ¯ carcinoma alVeolar ridge
¯ ameloblaStoma ¯ carcinoma oral tongue
¯ toruS ¯ carcinoma floor of mouth
¯ Pyogenic granuloma ¯ carcinoma buccal mucoSa
¯ irritation fibroma Verrucous Carcinoma
¯ mucocele ¯ carcinoma hard Palate
¯ ranula ¯ carcinoma retromolar trigone
¯ dermoid cyStS ¯ minor SaliVary gland tumorS
carcinoma of oral caVity ¯ melanoma
¯ lymPhoma
Epidemiology ¯ KaPoSi’S Sarcoma
Risk Factors ¯ clinical highlightS
Molecular Biology
Premalignant Lesions
Subsites of Oral Cavity
introduction benign tumorS of oral caVity
The tumors of oral cavity can be classified into two major
categories: benign and malignant. Benign tumors and tumor- PaPilloma
like lesions can be further divided into two groups: solid and Squamous papilloma is usually associated with human
cystic. Tori and dermoid cysts are congenital lesions. Malignant
tumors have two histopathological types: carcinoma and papillomavirus (HPV)-6 and HPV-11 virus subtypes. It is one
sarcoma (Box 1). of the most frequently occurring conditions.
402 box 1: Tumors of the oral cavity
Section 4 w oral cavity and Salivary glands • Benign fig. 1: Hemangioma tongue
– Solid
◊ Papilloma Hemangiomas that are large and persistent and continue
◊ Pleomorphic adenoma to grow need treatment. The sclerotherapy, cryosurgery
◊ Hemangioma and laser have not been found useful. Microembolization
◊ Lymphangioma alone or as a preoperative adjunct to surgery has been
◊ Granular cell tumor found useful.
◊ Ameloblastoma Phlebectasias are dilated veins, which occur on the oral or
◊ Torus (congenital) lingual mucosa in 40–50 years patients.
- Torus palatinus
- Torus mandibularis lymPhangioma
◊ Inflammatory The most common site of lymphangioma is anterior two-
- Pyogenic granuloma
- Irritation fibroma thirds of tongue.
– Cystic The lesion may be either diffuse (macroglossia) or localized
◊ Mucocele
◊ Ranula compressible soft swelling.
- Simple Treatment: Small lesions are totally excised. In large diffuse
- Plunging
◊ Dermoid cysts (congenital) lesions total excision is not advised. Partial excision reduces
- Sublingual the bulk.
- Submental
granular cell tumor
• Malignant Earlier it was thought to arise from the muscle and was
– Carcinoma
◊ Squamous cell carcinoma called myoblastoma. Now it has been reported to be
◊ Nonsquamous cell carcinoma derived from Schwann cells.
- Minor salivary gland tumors Most common site is tongue. Other sites include soft palate,
- Melanoma uvula and labial mucosa.
- Lymphoma It presents as a firm, painless, relatively immobile sessile less
– Sarcoma than 1.5 cm submucosal nodule.
◊ Kaposi’s sarcoma Congenital epulis, which is a granular cell tumor, involves
the gums of future incisors in female infants.
The peak incidence is in the third to fifth decades. Treatment: Excision biopsy. Recurrence is less than 10%.
Most common sites are soft and hard palate, uvula, tongue,
ameloblaStoma
lips and buccal mucosa. It is the most common neoplasm of odontogenic origin.
Mostly, they are pedunculated and white in color and less It is believed to arise from rests of primitive dental lamina,
than 1 cm in size. Their surface is usually wart like but in which is related to the enamel organ in alveolar bone.
some cases it is smooth. Patients are usually in third decade of life.
Treatment: Surgical excision or ablation with CO2 laser. Most common site is molar/ramus area of mandible.
CT scan shows unilocular or multilocular radiolucency with
PleomorPhic adenoma
It is the most common variety of minor salivary gland cortical bone expansion.
Treatment: En bloc resection with at least 1 cm margins of
benign neoplasms.
It usually involves soft and hard palate but can involve any normal appearing tissue.
Recurrence rate is 22%.
part of oral cavity. Malignant transformation is rare.
It presents as a painless progressive submucosal tumor.
Treatment: It needs wide excision because the recurrence
rate is high.
hemangioma
Oral cavity mucosal hemangiomas (Fig. 1) represent 14% of
all hemangiomas. They are mostly seen in children.
Most common site is lip.
Present as a soft, painless, red or blue mass of usually < 2
cm size. Extensive lesions involve significant portions of oral
cavity and oropharynx.
An infected hemangioma may look similar to a pyogenic
granuloma.
Treatment: Congenital hemangioma usually does not need
any treatment as the spontaneous regression is wellknown.
toruS 403
Torus is a frequently observed developmental anomaly. It
presents as a bony outgrowths in the second decade of life. It
continues to grow slowly throughout the life.
clinical features chapter 37 w neoplasms of the oral cavity
Tori are more common in females.
These pedunculated or multilobulated broadly based
smooth bony masses are usually asymptomatic.
In later life, they may interfere with denture placement and
get repeatedly injured while eating.
Torus palatinus is found in the midline of hard palate.
Torus mandibularis is found on the lingual surface of
mandible in the premolar region.
treatment fig. 2: Mucous retention cyst of lower lip
Removal from the underlying cortex with osteotomes or Plunging ranula is quite big and extends into the neck.
cutting burrs.
Pyogenic granuloma treatment
This reactive granuloma usually occurs in response to Excision: Small ranula may be completely excised.
Marsupialization: Large ranula needs marsupialization. It is
trauma or chronic irritation.
It mostly involves anterior gingivae but can be seen over difficult to excise the ranula completely. The thin wall and
ramifications of ranula go in various tissue planes.
tongue, buccal mucosa or lips.
It presents as soft smooth reddish to purple raised or pedun- dermoid cyStS
Dermoid cysts are lined by keratinized squamous epithe-
culated mass, which bleeds on touch.
Pregnancy granuloma or Epulis gravidarum is similar to lium. They are formed from epithelial rests that are found
along embryonic fusion lines. They contain elements of
pyogenic granuloma. It starts in the first trimester of preg- epidermal appendages such as hair follicles, sweat glands
nancy and regresses after the pregnancy. and connective tissue.
Epulis granulomatosa occurs after tooth extraction. Head and neck accounts for about 7% of total dermoid
Treatment: Excisional biopsy and removal of potential cysts; of this, 6.5–23% are found in floor of the mouth.
traumatic or infective factor. Recurrence is uncommon. As they enlarge, difficulties in deglutition, speech and
Pregnancy granuloma needs excision if persists after preg- respiration occur.
nancy. During pregnancy, it is not removed as the recur- There are two types of dermoids in this region: sublingual
rence rate is very high. and submental.
Sublingual dermoid is situated above the mylohyoid.
irritation fibroma
This common tumor-like condition of oral cavity is found – It can be either median or lateral.
– It shines as a white mass through the mucosa.
in 1.2% of adults. Submental dermoid develops below the mylohyoid
It usually becomes apparent during or after fourth decade. muscle.
Asymptomatic solitary sessile or pedunculated firm mass – It presents as a submental swelling.
Treatment: Complete excision of the cyst.
which is seldom larger than 1.5 cm.
Sites are buccal, labial or tongue mucosa.
History of chronic irritation is present.
Treatment: Conservative excisional biopsy.
mucocele carcinoma of oral caVity
This is a soft cystic bluish color retention cyst of minor
epidemiology
salivary gland. The five most frequent cancers in Indian males (in descending
Though it can occur anywhere in oral cavity, its most order) are mouth/oropharynx (Fig. 3), trachea/bronchus/lungs,
lymphomas/multiple myeloma, esophagus, and leukemia. In
common site is the lower lip (Fig. 2). women, they are (in descending order) breast, cervix, ovary,
Treatment: Surgical excision. mouth/oropharynx, esophagus, and lymphomas/multiple
myeloma (Source: ICMR, 2004). The incidence rate of oral cancer
ranula in India is very high (44.8 males and 23.7 females in 100,000
Ranula, a cystic grayish translucent swelling occurs in the population) in comparison to 11.2 of USA. This preventable
disease is caused by tobacco, alcohol, paan, reverse smoking,
lateral part of the floor of mouth and pushes the tongue up. areca nut and betel quid.
Ranula is the result of obstruction of the ducts of sublingual
salivary gland.
404 Hot spicy food
Xeroderma pigmentosa
Chronic glossitis
Cirrhosis.
Section 4 w oral cavity and Salivary glands fig. 3: Oral cavity overview molecular biology
risk factors The cases of oral verrucous carcinoma that expressed H-ras
The risk factors, which are associated with the development of gene also demonstrated evidence of HPV DNA (deoxyribo-
oral cavity cancers, include several Ss such as smoking, spirit, nucleic acid).
sopari (areca nut), sharp and septic tooth, syphilitic glossitis and
syndrome Plummer-Vinson. Tobacco and alcohol are the most Human papillomavirus is a mucosotropic virus. HPV onco-
common preventable factors. proteins E6 and E7 can degrade tumor suppressor gene
Smoking: Incidence of oral cancer is six times more in smokers. products of p53 and pRB, respectively. Significant increase
in HPV DNA was found within oral cavity carcinoma cases.
Reverse smoking, where burning end of the “churat” (rolled HPV-6 and HPV-16 were found risk factors for oral cavity
tobacco leaf) is put in the mouth, gives still higher incidence carcinoma independent of age and tobacco and alcohol
of cancer of the hard palate. Pipe smoking has been associ- use. HPV (OR-3.7) was found a risk factor for carcinoma,
ated with lip cancer. Forty percent of patients who continue independent of tobacco (OR-2.63) and alcohol (OR-2.57)
smoking after definitive treatment develop recurrence or use.
second head and neck malignancy.
Alcohol: Cancer of upper aerodigestive tract occurs six times Tumors negative for glutathione S-transferase (GST-π)
more in heavy drinkers. Individuals who both smoke and biomarker were found more responsive to cisplatin and
drink have 35 times more risk. Alcoholic mouthwashes have 5-fluorouracil.
also been implicated.
Chewing of paan, sopari and tobacco: Paan (specially Lack of bel-2 expression found consistent with an improved
prepared leaf ), sopari (betel nut, product of Areca catechu 3-year disease-free survival.
tree), quid (powdered tobacco mixed with lime) are placed
in the mouth and carcinoma develops at the site of their Studies suggest role of p53, EGFR, transforming growth
lodgment. This bad habit is largely responsible for oral factor (TGF)-a, and cyclin D1 in predicting prognosis of
cancer in Indians. Betel nut is a mild stimulant similar to head and neck carcinoma.
that of coffee.
Avitaminosis and malnutrition: Riboflavin deficiency is Premalignant lesions
proposed to be responsible for cancer in alcoholics.
Dental caries, sharp jagged teeth and ill fitting dentures: They Lichen planus: It has been associated with lip cancer. In cases
cause chronic irritation, which may result in malignant of erosive lichen planus or atrophic lichen planus, there is
change. risk of malignant change (see Chapter 35: Oral Mucosal
Human papillomavirus: The role of HPV has been in a subset Lesions).
of head and neck squamous cell carcinoma.
Environmental ultraviolet light exposure: It has been associ- Syphilis: The syphilitic interstitial glossitis with an endarteritis
ated with lip cancer. causes atrophy of the overlying epithelium that is more
Long-term immunosuppression: There is 30 fold increased vulnerable to carcinogenic irritants. Patients need treatment
risk with renal transplant. of syphilis and regular follow-up.
HIV infection: Kaposi’s sarcoma may occur in oral cavity.
Other carcinogenic factors proposed in the etiology are Plummer-Vinson syndrome or Paterson-Kelly syndrome or
following: Sideropenic dysphagia: It consists of achlorhydria, iron
deficiency anemia, and mucosal atrophy of mouth, pharynx
and esophagus. The oral mucosa becomes thin, pale and
atrophic. The disease is particularly common in women. It is
said to be a premalignant condition and may be responsible
for cancer of the oral cavity and post cricoid region. The
epithelial atrophy is extremely vulnerable to carcinogenic
irritants. Anemia responds to iron supplements.
Dyskeratosis congenita: This syndrome consists of
Reticular atrophy of skin with pigmentation
Nail dystrophy
Oral leukoplakia with thickened, fissured and white
mucosa.
Leukoplakia (see Chapter 35: Oral Mucosal Lesions).
Erythroplakia (see Chapter 35: Oral Mucosal Lesions).
Chronic hyperplastic candidiasis (see Chapter 35: Oral
Mucosal Lesions).
Discoid lupus erythematosus (see Chapter 35: Oral Mucosal
Lesions).
Submucous fibrosis (see Chapter 35: Oral Mucosal Lesions).
Subsites of oral cavity Reconstruction: Primary reconstruction is now the rule. 405
The current techniques of reconstruction include
The oral cavity extends from the lips to the level of anterior – Muscle flaps: Pectoralis major, trapezius, and latis- chapter 37 w neoplasms of the oral cavity
tonsillar pillar. Subsites of cancer in oral cavity are (Source: simus dorsi
AJCC, 1997) (Fig. 3): – Microvascular techniques: Free tissue transfer.
Lip (Vermilion surface)
Management of neck
Upper lip N0: A function sparing elective neck dissection, in which
Lower lip accessory nerve, internal jugular vein (IJV) and sternoclei-
Commissures domastoid muscle are preserved, is advocated in tumors
Buccal mucosa (includes mucosa of cheek and inner surface of floor of mouth, lower alveolus and tongue. In presence
of lips up to line of contact of opposing lip): Mucosal of 2 or more positive nodes or extracapsular spread post-
surfaces of operative radiotherapy is given. Over 96% of histologi-
Upper and lower lips cally positive nodes can be removed by supra-omohyoid
Cheeks dissection. Alternatively, elective irradiation of clinically
Retromolar area negative neck prevents subsequent nodal disease.
Upper and lower buccoalveolar sulci N1/N2a/N2b: Radical neck dissection followed by post-
Anterior two-third of tongue (anterior to vallate papillae) operative radiotherapy. In inoperable cases, radical
Dorsal and ventral surfaces external beam irradiation.
Lateral borders N2c: In young operable cases, full radical neck dissection
Tip on the ipsilateral side and IJV sparing neck dissection
Hard palate on contralateral side followed by postoperative radio-
Lower alveolar ridge (alveolus and gingiva) therapy. Radical radiotherapy is advocated in inoperable
Upper alveolar ridge (alveolus and gingiva) cases.
Floor of mouth N3: External radiotherapy.
Retromolar trigone. Lymph node metastasis after primary treatment: After
confirming by fine-needle aspiration cytology, radical
clinical evaluation and investigations neck dissection is done followed by postoperative
radiotherapy.
For history taking, clinical evaluation, investigation and imaging
studies, see chapter Oral Symptoms and Examination in the External beam radiation and brachytherapy
section of Oral Cavity and Salivary Glands. Adjunctive chemotherapy
Photodynamic therapy
Staging Organ preservation protocols
Table 1 shows TNM classification. Chemoprevention
Speech and swallowing rehabilitation
histopathology Pain management
Palliative care.
Most of the oral cavity malignant growths (85%) are squamous
cell carcinoma and are mainly managed surgically. Other • Skin cancers: Surgical excision is the treatment of choice.
malignancies in decreasing frequency are minor salivary gland • Healing: Primary closure of a facial defect is best if possible.
tumors, lymphomas, malignant melanomas, sarcoma and
metastatic tumors. Other options include healing by secondary intention, local
flaps, skin grafts and regional or free flaps.
treatment
Multidisciplinary tumor conference, which consists of head and The factors, which help in deciding the optimum manage-
neck and plastic surgeons and radiation and medical oncolo- ment for a patient, includes following:
gists, decides the best line of management. The treatment Site and TNM stage: An alveolar lesion and other sites small
options include following:
Primary tumor including mandible/maxilla lesions (T1) and neck node metastasis (N1 and N2) are best
managed by surgery. The management of most T2 and early
Early lesions T1/T2: Transoral complete removal of tumor T3 tumors is controversial.
with adequate margin followed by primary closure, Histology: Adenocarcinoma and melanoma are relatively
healing by secondary intention, or skin-dermal graft. radioresistant and are preferably treated surgically. Early
verrucous carcinoma is suitable for local excision. Advanced
Larger or more posterior lesions: They need pull through verrucous carcinoma is treated as squamous carcinoma.
technique for exposure and reconstruction. Lip splitting General: Age, medical condition and life style of the patient.
and mandibulotomy facilitates safe resections of tumors
in tongue and floor of mouth in continuity with neck Prognosis
lymphatics. In spite of advancing technology and surgical procedures
during the last 40 years the 5-year cure and survival rate has
Mandible involvement: Marginal, segmental or hemi- remained about 55%.
mandibulectomy. Rim resection avoids mandibular Second primary: The longer a patient survives greater is the
discontinuity without risking local recurrence.
risk of developing second primary tumor in the oral cavity,
larynx, bronchus or esophagus.
406 table 1 AJCC Cancer Staging and UICC TNM classification of oral cancer
Primary tumor (T)
Tx Unable to assess primary tumor
T0 No evidence of primary tumor
Tis Carcinoma in situ
T1 Tumor is < 2 cm in greatest dimension
T2 Tumor > 2 cm and < 4 cm in greatest dimension
T3 Tumor > 4 cm in greatest dimension
T4 (lip) Primary tumor invading cortical bone, inferior alveolar nerve, floor of mouth, or skin of face (e.g., nose or
chin)
T4a (oral) Tumor invades adjacent structures (e.g. cortical bone, into deep tongue musculature, maxillary sinus) or
skin of face
T4b (oral) Tumor invades masticator space, pterygoid plates, or skull base or encases the internal carotid artery
Section 4 w oral cavity and Salivary glands Regional lymphadenopathy (N)
Nx Unable to assess regional lymph nodes
N0 No evidence of regional metastasis
N1 Metastasis in a single ipsilateral lymph node, <= 3 cm in greatest dimension
N2a Metastasis in single ipsilateral lymph node, > 3 cm and < 6 cm
N2b Metastasis in multiple ipsilateral lymph nodes, all nodes < 6 cm
N2c Metastasis in bilateral or contralateral lymph nodes, all nodes < 6 cm
N3 Metastasis in a lymph node > 6 cm in greatest dimension
Distant metastases (M)
Mx Unable to assess for distant metastases
M0 No distant metastases
M1 Distant metastases
TNM staging
Stage 0 Tis N0 M0
Stage I T1 N0 M0
Stage II T2 N0 M0
Stage III T3 N0 M0; T1-3 N1 M0
Stage IVA T4a N0-1 M0; T1-4a N2 M0
Stage IVB T4b N0-2 M0; T1-4b N3 M0
Stage IVC T1-4b N1-3 M1
Source: American Joint Committee on Cancer (AJCC) Staging Manual, 6th edition. Chicago; 2002
Metastasis via blood stream: It is relatively an early event in to submandibular nodes. Upper lip drains into preauricular,
oral cancer. infraparotid and submandibular nodes.
Factors affecting prognosis: They include: clinical features
Infiltrative growths have comparatively poorer prognosis. Sex: Males in the age group of 40–70 years are more affected.
Depth of invasion: More the depth of invasion higher Lesion: Exophytic or ulcerative type.
the risk of regional metastasis and poorer the 5-year Most common site: Between the midline and commissure
survival.
Stage: Higher the stage, poorer is the 5-year survival. of the lower lip.
Histopathology: The following histopathologic findings Local spread: Initially tumor spreads laterally and later infil-
have prognostic significance:
– Keratin production trates deeply and spread into anterior triangle of neck and
– Level of differentiation invade mandible.
– Nuclear appearance Regional lymphatic metastasis: It is late and develops into
– Mitoses submental and submandibular nodes. At later stage, deep
– Inflammation cervical group of lymph nodes may get involved.
– Desmoplastic reaction Histopathology: Mostly, squamous cell carcinoma.
– Patterns of invasion
– Vascular invasion treatment
carcinoma liPS Either radiation therapy or surgery for stage I tumors gives
cure rates greater than 85%. Surgery for large tumors consists
Lips form the anterior boundary of the vestibule. Medial of excision with adequate safety margin and repair. Block
portion of lower lip drains into submental and lateral portion dissection is done if lymph nodes are involved. Postoperative
radiotherapy to chin and neck region is planned in high-risk
advanced stage tumors.
Leukoplakia lip or actinic cheilitis: Leukoplakia or actinic 407
changes on the vermilion border of lip due to ultraviolet
radiations can be managed with either lip shave or laser. a chapter 37 w neoplasms of the oral cavity
The resection is reconstructed either by advancing labial
or buccal mucosal flaps or use of pedicled anteriorly based
tongue flap.
2 cm lesion of lower lip: Up to one-third of lower lip can
be removed with a V or W shaped excision with primary
closure in three layers (mucosa, muscle and skin) under local
anesthesia as an OPD procedure. Initially lip looks tight but
improves after 3 months.
Reconstruction: More extensive lip resection needs local
flaps for reconstruction.
For large central defects of lower lip: Step ladder
approach of Johnson advances symmetrical bilateral
flaps from lower third of face.
For large lateral defects of lower lip, upper lip involving
commissure: Fries’s “universal procedure”, in which
lateral flaps are developed following full-thickness
incisions in the cheeks parallel to the branches of facial
nerve. The flaps are then advanced into the lip defect.
The Fries modifications of the Bernard flap can be used
for total reconstruction of both lower and upper lips.
carcinoma gingiVa/alVeolar ridge b
Gums (gingivae) surround the teeth and cover the upper and
lower alveolar ridges. figs 4a and b: (A) Carcinoma left lower alveolus (premolar to
retromolar region) extending to buccal mucosa, floor of mouth
Buccal aspect of mucosa drains into submental and and cheek skin; (B) Note the lower jaw swelling and pus from
submandibular nodes. Lingual aspect of upper alveolus drains skin lesion
into upper deep cervical and lateral retropharyngeal nodes.
Lingual aspect of lower alveolus drains into submandibular Upper alveolar tumor involving inferior structure of maxilla
nodes. requires total maxillectomy followed by postoperative
radiotherapy.
clinical features
The history of failure of socket healing after tooth extrac- Primary reconstruction should always be undertaken.
tion is common. carcinoma oral tongue
The history of sudden difficulty in wearing denture is Anterior two-third of tongue is the content of the oral cavity.
Posterior one-third (base of tongue) is situated behind the
common. circumvallate papillae and forms anterior wall oropharynx.
Superficial ulceration or proliferative tissue at the gingival Oral tongue can be divided into different regions: tip, lateral
borders, dorsum and the undersurface.
margin.
Most common site is the lower jaw in the premolar region Tip of tongue drains into submental and jugulo-omohyoid
nodes. Lateral portion drains into ipsilateral, submandibular
and just behind the first molar (Figs 4A and B). and deep cervical nodes. Central portion and base drain into
Local spread: To cheek, floor of mouth, retromolar trigone deep cervical nodes of both sides.
and hard palate. After invading underlying bone, it spreads gross Pathology
rapidly along the neurovascular bundle. Pre-existing lesions: Some patients have pre-existing leuko-
Nodal metastases: The enlargement of submandibular and
upper jugular nodes is common at the time of presentation. plakia, dental ulcer or syphilitic glossitis.
Common site: Middle third of the lateral border. Figures 5 to
treatment
Surgery is preferred over radiotherapy. Radiations lead to radio- 8 show three different types of lesions. The lesion extends
osteonecrosis. early on to the ventral surface of the tongue and floor of
Early lesion on the lower alveolus is excised (marginal resec- mouth. The tip and dorsum are uncommon sites (Fig. 9).
tion of the mandible).
Extensive tumor of lower alveolus requires segmental
or hemimandibulectomy. Access is achieved via lip split
approach. Block dissection is needed when lymph nodes
are involved.
Tumors confined to hard palate, upper alveolus and floor
of maxillary antrum needs partial maxillectomy with block
dissection if nodes are enlarged.
408
Section 4 w oral cavity and Salivary glands fig. 5: Carcinoma tongue right lateral margin. Nodular lesion
with induration of the surrounding tissue
Local spread: Deeply into the musculature (causes ankylo- fig. 6: Carcinoma tongue right lateral margin. Ulcerative lesion
glossia), inferiorly into the floor of mouth and laterally into with rolled edges and grayish white shaggy base with induration
alveolus and mandible.
Lymph node metastases: Lateral border of tongue drains
into submandibular and upper jugular nodes (Fig. 8). Tip
of tongue drains to the submental and jugulo-omohyoid
group. Bilateral and contralateral lymph node involvements
can occur.
Histopathology: Squamous cell carcinoma is most common.
clinical features fig. 7: Malignancy tongue. Nonhealing ulcer with infiltration. The
This is commonly seen in 50–70 years of men. ulcer may be present superficially or in depths of a fissure infil-
Early lesions are painless and may remain asymptomatic.
trating underlying muscle
Lesion arises in an atrophic depapillated area with an
erythroplakia patch with peripheral streaks or areas of Stage I (T1 N0): Equal results with radiotherapy or surgery.
leukoplakia. Simple intraoral excision is preferred. Formal reconstruction
Painful ulcer/growth/lump is a late feature. is not required if less than one-third of the tongue is excised.
Referred earache occurs due to common nerve supply
(branches of mandibular division of trigeminal) of the Stage II (T2 N0): Treated by radiotherapy (including tumors
tongue (lingual nerve) and ear (auriculotemporal). and regional lymph nodes) or by surgical excision
Enlarged lymph node presents as mass in the neck (Fig. (Hemiglossectomy) with prophylactic neck dissection.
8). About 50% patients have palpable nodes at the time of
presentation. About 12% of the patients present with only Stage III or IV: Hemiglossectomy (depending on the extent
lump in neck. of the tongue lesion) combined with marginal, segmental
Late features: Dysphagia, odynophagia (leads to drooling of or hemimandibulectomy (depending upon the extent of
saliva), ankyloglossia, slurred speech, bleeding, cachexia. involvement of mandible) and radical neck dissection of
Lesion: Often, the lesion is exophytic with areas of ulcer- lymph nodes (commando operation) followed by postopera-
ation. tive radiotherapy.This strategy gives better results than either
Exophytic: An exophytic lesion like a papilloma.
Ulcerative: A nonhealing ulcer with rolled edges (Fig. 6)
and grayish white shaggy base with induration. The ulcer
may be present superficially or in depths of a fissure infil-
trating underlying muscle (Fig. 7).
A submucous nodule with induration of the surrounding
tissue.
The lesion may be associated with leukoplakia.
treatment
The main modalities of treatment, which depends on the
staging of the cancer (Table 1), are surgery and radiotherapy.
One should try to preserve function of the tongue along with
the total eradication of cancer as far as possible.
409
fig. 8: An advanced case (Stage IV: T4 N3) of right side carci- fig. 10: Intraoral view—Operated case of carcinoma tongue chapter 37 w neoplasms of the oral cavity
noma tongue (tumor invades into deep tongue musculature) with right lateral margin involving middle and posterior one-thirds with
secondary neck node at level II. The local wide excision included
secondary neck nodes (lymph node > 6 cm in greatest dimen- right tongue margin, floor of mouth, tonsillar pillar, and alveolar
marginal mandibular resection with modified neck dissection
sion)
fig. 9: Carcinoma tip of tongue with trismus due to oral submu- fig. 11: External neck incision of the patient shown in Figure 11
cous fibrosis
surgery or radiotherapy alone. A rim mandibular resection is carcinoma floor of mouth
advised when lesion reaches but does not invade alveolus
(Figs 10 and 11). Floor of mouth is a crescent-shaped area that lies between the
Approach: In cases of extensive tongue lesions involving gingivae and undersurface of tongue. Anterior portion of the
floor of mouth and alveolus, access is best via a lip split and floor (frenulum, sublingual papillae with openings of subman-
mandibulotomy. The traditional pull-through procedure dibular ducts) is examined when patient raises the tip of tongue
does not allow adequate excision. towards the hard palate. Lateral portion of floor of mouth is
Reconstruction: examined by displacing the tongue in medial direction with
Radial forearm free flap with microvascular anastomosis: the help of a tongue depressor.
When tongue defect does not exceed two-third of the Anterior portion of floor of mouth drains into submental
original tongue. and submandibular nodes. Lymphatics from this area also
Pectoralis major muscle flap: For very large defects, total cross the midline. Posterior portion drains into upper deep
glossectomy or deeply infiltrating lesions when resec- cervical nodes.
tion extends to hyoid bone.
410 clinical features
Male/Female ratio: Males are affected more than females
Section 4 w oral cavity and Salivary glands fig. 12: Malignancy buccal mucosa in pre-existing erythroleu-
(ratio of 4:1). koplakia lesion at angle of mouth and in the plane of occlusion
Early features: Lesion may remain asymptomatic or cause
Patient develops trismus if buccinator, masseter, or
soreness or irregularity in the floor of the mouth. medial pterygoid muscle is involved.
Submandibular swelling: It may be due to either enlarged
If the lesion spreads radially, it involves angle of the
submandibular salivary gland or lymph node metastases. mouth and lip anteriorly; retromolar trigone and medial
Lesion: Ulcerative or infiltrative lesion. pterygoid muscle posteriorly; upper gingivobuccal
Leukoplakia: It is more common in the floor of mouth than sulcus and maxilla superiorly; and lower gingivobuccal
sulcus and alveolar ridge and gums inferiorly.
at other sites.
Common site: Begins anteriorly near the opening of subman- Lymphatic spread: Submandibular, submental, and parotid
nodes. Later on upper jugular nodes are affected. In some
dibular duct that get obstructed and lead to enlargement cases, there occurs direct involvement of upper jugular
of submandibular gland. nodes skipping the submandibular group. Nodal involve-
Local spreads: Ventral aspect of the tongue, lingual gingiva, ment develops in about 50% cases.
mandibular periosteum or deeply into the floor of mouth
and submental space. Histopathology: Squamous cell carcinoma is most common
Lymphatic metastases: Submandibular and jugulodigastric but salivary gland tumors are also seen.
nodes and may be bilateral
Histopathology: Usually squamous cell carcinoma. clinical features
Early lesions are asymptomatic.
treatment Pain and bleeding.
Stage I: If there is no involvement of tongue, lingual gingiva Trismus: Involvement of buccinator, masseter or pterygoid
or nodes than small lesions are treated with wide excision muscles leads to trismus (Fig. 13).
or radiotherapy, which offer equal results. Late feature: Fungating foul smelling bleeding mass over
Stage II: Prophylactic neck dissection or irradiation is done
for stage II cancer because there is high incidence of micro- the cheek or in the oral cavity (Figs 14 and 15).
metastases (40%).
Stage III and IV: These patients need surgery and radio-
therapy. Large tumor with involvement of tongue, gingiva,
mandible and nodes require hemiglossectomy, marginal or
segmental mandibular resection, and radical neck dissec-
tion. Resultant defect is reconstructed with either a local
or distant flap.
carcinoma buccal mucoSa
Buccal mucosa lines the inner surface of cheeks and lips and
extends between the superior and inferior gingivobuccal
sulcus. It extends posteriorly up to pterygomandibular raphe
and anteriorly to the meeting line of lips. Buccal mucosa drains
into submental and submandibular nodes.
Carcinoma of buccal mucosa is the second most common
cancer of oral cavity after the tongue.
Pathology Verrucous carcinoma
Mostcommonsites: Angle of mouth and the plane of occlusion
Verrucous carcinoma appears as soft white velvety area of
(Fig. 12) to retromolar region. Gingivobuccal sulcus where paan superficial proliferative exophytic lesion (like a white papil-
or tobacco quid is kept is not uncommon. lary growth), which has considerable keratinization.The deep
Multicentric: Buccal mucosa cancer may be multicentric as invasion and induration are minimal. The tumor behaves like a
the entire buccal mucosa is “condemned”. low-grade squamous cell carcinoma. The lymph node metas-
Lesion: tasis is late.
Exophytic lesions are associated with erythroleuko-
treatment
plakia (Fig. 12).
Ulceroinfiltrative lesions may infiltrate deeply. Stage I (T1 N0): Wide excision with safety margin including
Verrucous carcinoma. underlying buccinator muscle followed by quilted split-
Local spread: skin graft.
The ulcer may spread deeply and involves different
Stage II (T2 N0): Radiotherapy to the primary lesion and
layers of cheek such as submucosa, muscle, subcuta- regional lymph nodes if bone is spared. If bone (maxilla and
neous fat and skin.
411
fig. 13: Malignancy buccal mucosa right side with trismus ab chapter 37 w neoplasms of the oral cavity
figs 15a and b: Coronal (A) and Axial (B) T2W MR images.
Hyperintense mass in left buccal mucosa along upper and lower
alveolus. Underlying bone shows normal marrow signal intensity
Source: Dr Swati Shah, Professor, Radiodiagnosis, GCRI Medi-
cal College, Ahmedabad
Buccal fat pad with or without temporalis muscle flap: For
reconstruction of maxillary defects, hard and soft palate
defects, and cheek and retromolar defects.
carcinoma hard Palate
It is common in India as some people have the bad habit of
reverse smoking (keeping the burning end of bidi or cigar
in the mouth). Hard palate forms the roof of the oral cavity.
Hard palate drains into the upper deep cervical and lateral
retropharyngeal nodes. Anterior part of palate drains into
submandibular nodes.
Hard palate contains high number of minor salivary glands.
Minor salivary glands tumors (adenoid cystic, mucoepider-
moid and adenocarcinoma) are more common than squamous
cell carcinoma. Most of the squamous cell carcinoma of upper
alveolus and hard palate arises from maxillary antrum.
fig. 14: Carcinoma buccal mucosa. Contrast CT scan neck axial clinical features
section. Enhancing thickening of right buccal mucosa (12–14 mm Lesion: Superficial ulcer with rolled out edges, which may be
thickness) with mild stranding of adjacent buccal planes
Source: Dr Ritesh Prajapati, Consultant Radiologist, Anand, Gu- felt by tongue as painless irregularity on the palate.
jarat Local spread: To gingiva, lip, soft palate. The invasion of hard
palate can involve floor of the nasal cavity and the maxillary
antrum (Fig. 16). This condition should be differentiated
from cancer of maxillary antrum and nose, which could
spread to and involve hard palate.
Lymphatic metastasis: It is late and involves submandibular
and upper jugular nodes and indicates poor prognosis.
mandible) is involved or growth infiltrates the muscle, exci- treatment
sion of the growth combined with marginal or segmental Small tumors are excised along with the hard palate.
mandibulectomy or partial maxillectomy along with the Tumors confined to hard palate, upper alveolus and floor
reconstruction.
Stage III and IV: Surgical resection combined with neck of maxillary antrum needs partial maxillectomy with block
dissection and reconstruction and postoperative radio- dissection if nodes are enlarged.
therapy. Surgical defect in the palate needs closure or a suitable
Reconstruction: prosthesis.
Free radial forearm flap: Lesion extending to retromolar
carcinoma retromolar trigone
area, maxillary tuberosity or tonsillar fossa. Retromolar trigone is a triangular area of mucosa that covers
anterior surface of the ascending ramus of mandible. Its base
412 Males are affected double than females.
The most common age of presentation is sixth decade.
Initial asymptomatic melanomas are usually raised or
nodular lesions. They may be flat.
Lesion: The area of higher pigmentation varies from black
to brown and present for many years. It ulcerates, bleeds
and becomes painful. Amelanotic (nonpigmented) variety
is red in color and rare (15%).
The rapid growth is associated with destruction of under-
lying bone.
Both the regional lymph node and distant metastases are
seen. About 50% patients have metastases at the time of
presentation.
Section 4 w oral cavity and Salivary glands treatment
Wide surgical excision followed by radiotherapy.
fig. 16: Carcinoma left side hard palate crossing midline and Prognosis
extending to alveolus and floor of nasal cavity Recurrence is quite common.
Prognosis is very poor (5-year survival only 5%). Indicators
lies posterior to the last molar while its apex is adjacent to the
maxillary tuberosity. of poor outcome are following:
It may be either primary or secondary (extension of growths Main guide to prognosis: Histological tumor thickness
from the gingiva, floor of mouth, buccal mucosa or the (Breslow) in mm from the granular cell layer to the
palate). deepest identifiable melanocyte.
Depending on the extent of lesion, wide surgical excision Malignant melanocytes in blood vessels.
with block dissection is done. Multiple or atypical mitoses.
Destruction of underlying bone.
minor SaliVary gland tumorS Presence of metastases.
Minor salivary gland tumors are mostly malignant (adenoid
cystic carcinoma 40%, adenocarcinoma 30% and mucoepider- KaPoSi’S Sarcoma
moid carcinoma 20%). This vascular tumor is seen in acquired immune deficiency
Most common site is palate. Other sites are tongue, cheek,
syndrome (AIDS) patients.
lip, gums and floor of mouth. It is multifocal in origin and primarily affects skin but may
Treatment: Wide surgical excision along with block dissec-
also be seen in the oral cavity.
tion, if nodes are involved. It presents as a reddish purple nodule or a plaque mostly
melanoma on the palate.
They are rare in oral cavity and oropharynx. The tumor consists of spindle cells with hemorrhagic cleft-
Most common sites are palate (50%) and upper gingiva
like spaces.
(25%). Chemotherapy may offer good result in non-AIDS patients
but its response in AIDS patients is poor.
clinical highlights
1. minor salivary gland tumor: The most common site of minor salivary gland tumor is hard palate.
2. cancer tongue: Lateral border is the most common site for carcinoma of oral tongue. Patient develops referred earache
because the anterior two-third tongue receive its somatosensory innervation from the lingual nerve, which is branch of
mandibular division of the CN V. The best treatment for stage III carcinoma of oral tongue is wide excision with supra-
omohyoid neck dissection and postoperative radiotherapy.
3. Stage iii t2n1m0 carcinoma of buccal mucosa: The best treatment will be surgical excision of growth with supra-
omohyoid neck dissection and postoperative radiotherapy.
4. Abbey-Estlander flap: It is used to reconstruct defects in cases of carcinoma of lip angle (commissure). Such defects
require partial commissure reconstruction.
5. melanoma: Hard palate and maxillary gingiva are the most common sites of melanoma in the oral cavity.
further reading 413
1. Bahadur S. Oral cancer. Indian J Otolaryngol Head Neck Surg. 2005;Special issue-I:2-7. chapter 37 w neoplasms of the oral cavity
2. Hegde MC, Kamath PM, Shreedharan S, et al. Supravital staining: It’s role in detecting early malignancies. Indian J Otolaryngol Head Neck
Surg. 2006;58:31-4.
3. Hemaraju N, Nanda SK, Medikeri SB. Sublingual dermoid cyst. Indian J Otolaryngol Head Neck Surg. 2004;56:218-20.
4. Jagade M. Role of tobacco in oral carcinoma. Indian J Otolaryngol Head Neck Surg. 2005;Special issue-II:577-8.
5. Marathe D, Gupta S. Plunging ranula. Indian J Otolaryngol Head Neck Surg. 2005;Special Issue-I: 238-9.
6. Nilkantan A, Venkatesh MD, Raghavan D, et al. Management of the node negative early carcinoma tongue. Indian J Otolaryngol Head
Neck Surg. 2007;59:229-36.
7. Patil VG, Nagle SK, Jagade MV, et al. Reconstruction of mandible with free fibular vascular graft. Indian J Otolaryngol Head Neck Surg.
2003;55:49-50.
8. Prakash M, Bahadur S, Thakar A, et al. Role of tumor thickness in carcinoma of oral tongue with clinically negative neck. Indian J Otolar-
yngol Head Neck Surg. 2005;Special issue-I:8-12.
9. Sen R, Purwar P, Rekhi B, et al. Intra-oral minor salivary duct carcinoma. Indian J Otolaryngol Head Neck Surg. 2004;56:143-5.
10. Singh GB, Tiwari M, Shukla HS, et al. Nd: YAG laser therapy of carcinoma lip (stage I squamous cell carcinoma): a retrospective evaluation:
Indian J Otolaryngol Head Neck Surg. 2009;61:179-84.
11. Varshney PK, Agarwal N, Bariar LM. Tobacco and alcohol consumption in relation to oral cancer. Indian J Otolaryngol Head Neck Surg.
2003;55:25-8.
Section 5 : Pharynx and Esophagus
38 Pharyngeal Symptoms and
Examination
The injunctions of Destiny are canceled if one takes refuge in God. Destiny has to strike off with her own hand what she has
decreed about such a person.
— Holy Mother Sarada Devi
Points of Focus Esophagogram
Evaluation of Pharynx Oral Contrast Agents
¯¯Nasopharynx
¯¯Esophageal Manometry
Symptoms Indication
Examination
¯¯Oropharynx ¯¯Ambulatory 24-Hours Esophageal ph
Symptoms Recording
Examination Indication
¯¯Laryngopharynx
Evaluation of Esophagus Dysphagia
¯¯Barium Esophagography Odynophagia
Fluoroscopy
Cineradiography Causes
Video esophagography
Modified Barium Swallow ¯¯Evaluation
History
Physical Examination
Investigations
¯¯Clinical Highlights
Evaluation of Pharynx about the habits of chewing paan, sopari or tobacco,
smoking and alcohol.
For general scheme of case taking and general set-up of
Bull’s eye lamp light source and head mirror, see history NASOPHARYNX
and examination chapter in section of Basic Sciences. This upper part of pharynx lies behind the nasal cavity,
Pharyngeal symptoms include sore throat, ulcers, growth, and above the soft palate. Laterally, it communicates with
pain, odynophagia (painful swallowing), stridor, voice the middle ear through the Eustachian tube opening.
change, nasal voice, dysphagia (difficulty in swallowing),
snoring, cough, sputum, injury and foreign body. The Symptoms
associated complaints include fever, headache, earache, Symptoms of nasopharyngeal disorders include the
conductive hearing loss, vomiting, nasal regurgitation, following:
loss of weight and anorexia. Patient must be inquired
416 Nasal obstruction becoming obsolete with the advent of sinuscope and
Nasal discharge anterior or posterior flexible nasopharyngolaryngoscopy.
Section 5 w Pharynx and Esophagus Epistaxis Digital examination: Digital examination though uncom-
Conductive hearing loss fortable for the patient, is a simple method to palpate
Symptoms of cranial nerve palsies the nasopharynx. Examiner, standing behind and right to
Metastatic neck nodes. the patient invaginates patient’s cheek with his left finger
and introduces right index finger behind and above the
Examination soft palate into the nasopharynx. This method is usually
Box 1 shows the methods of examination and nasoph avoided in cases of angiofibroma.
aryngeal structures, and pathological findings seen during Endoscopy: Endoscopy gives a bright and magnified view
examination and their causes. Examination of cranial nerves of the nose and nasopharyngeal structures. It can be
and regional lymph nodes is important. The tumors of performed by either rigid or flexible fiber-optic scope.
nasopharynx can involve any of the cranial nerve from second Rigid nasal endoscope (sinuscope or rhinoscope):
through twelfth (often CN IX, X and XI), and cervical lymph They are available in different sizes and angles and
nodes (upper internal jugular, and along the accessory nerve). introduced through the nose after instilling or spraying
Anterior rhinoscopy: Some part of the nasopharynx can be local anesthetic and decongestant. See details of sinus-
copy examination in chapter Operations of Nose and
seen in decongested nose (with vasoconstrictors); even on Paranasal Sinuses.
anterior rhinoscopy. Flexible nasopharyngolaryngoscope: It offers views
Posterior rhinoscopy: Posterior rhinoscopy provides frag- of nose, pharynx and larynx. See chapter Laryngeal
mented view of nasopharynx, which is mentally reconsti- symptoms and Examination in section of larynx, trachea
tuted by the examiner. The examiner has to tilt the mirror and bronchus.
in different directions to visualize the structures present
on different walls of the nasopharynx. OROPHARYNX
Retraction of soft palate with catheters: It facilitates
Oropharynx lies behind the oral cavity, and includes tonsils
postnasal mirror examination in some difficult cases and their pillars, soft palate, base of tongue, and posterior
and requires good local or general anesthesia. In this pharyngeal wall (Fig. 1). It lies behind the anterior tonsillar
method, a soft rubber catheter is passed through each pillars, hard palate and V-shaped row of lingual circumvallate
nostril and then taken out from the mouth through the papillae.
oropharynx. Both ends of catheter are held together,
and pulled forward. Retraction of soft palate makes
the mirror examination easy. This method has been
Box 1: Examination of nasopharynx: Methods of examination, nasopharyngeal structures, and
pathological findings and their causes
•• Methods:
–– Anterior rhinoscopy
–– Posterior rhinoscopy
◊ Retraction of soft palate with catheters
–– Digital examination
–– Endoscopy: Sinuscope, flexible nasopharyngolaryngoscope
–– Examination of cranial nerves especially CN IX, X and XI
–– Examination of neck nodes especially upper internal jugular, and along the accessory nerve
•• Nasopharyngeal structures:
–– Anterior: Posterior border of nasal septum, choanae, posterior ends of turbinates and their meatuses
–– Lateral: Opening of Eustachian tube, torus tubarius, and pharyngeal recess (Fossa of Rosenmuller)
–– Floor: Upper surface of soft palate
–– Roof and posterior wall: Adenoids, median recess of nasopharyngeal bursa within the adenoid mass, Rathke’s pouch dimple
above the adenoids (junction of nasal septum and roof of nasopharynx)
•• Pathological findings and their causes:
–– Discharge: Middle meatus (infections of anterior group of sinuses), superior meatus (infections of posterior group of sinuses)
–– Crusting. Atrophic rhinitis or nasopharyngitis
–– Mass:
◊ Smooth pale mass (antrochoanal polyp)
◊ Pink lobulated mass (angiofibroma)
◊ Irregular bleeding mass (carcinoma)
◊ Smooth swelling in the roof (Thornwald’s cyst or abscess)
◊ Irregular mass with radiating folds (adenoids)
◊ Mulberry irregular mass filling the lower part of choana (hypertrophy of inferior turbinate)
–– Bleeding
crypts. The base of tongue is examined by laryngeal mirror. 417
The structures of oropharynx and their common lesions are
Fig. 1: Oropharyngeal structures seen through opened mouth mentioned in Box 3. Chapter 38 w Pharyngeal Symptoms and Examination
Tonsils and pillars: For expressing the material from tonsil
Symptoms
The lesions of oropharynx can disturb swallowing, phonation, crypts, pressure on the anterior pillar is applied with the
respiration and hearing. The common symptoms and their edge of tongue depressor. Palpation should always be
causes are mentioned in Box 2. performed with a gloved finger to know the consistency
Middle ear symptoms: A conductive hearing loss can occur of the mass. There is uniform congestion of the pillars,
tonsils and pharyngeal mucosa in acute tonsillitis; however,
due to Eustachian tube malfunction, which may result from congestion of only anterior pillars indicates chronic tonsil-
enlarged tonsils (interfere movements of soft palate), cleft litis. Ulcer and proliferative growth may extend to or from
palate and palatal paralysis. The infections of recurrent phar- the tonsil, base of tongue, and the retromolar trigone.
yngitis and tonsillitis can travel to the middle ear through Soft palate: In cases of peritonsillar abscess, uvula becomes
Eustachian tube. edematous, and displaced to the opposite side. To note
Cancer phobia: These patients may be concerned with some the movement of soft palate, patient is asked to say “AA”.
structure in the oropharynx, which is noticed while looking in Deviation of the uvula and soft palate occurs to the healthy
the mirror. Hypertrophic circumvallate or foliate papillae can side in cases of vagus palsy, which may be associated with
generate cancer fear in these patients who need reassurance. paralysis of posterior pharyngeal wall that manifests as
a “curtain effect” (the paralyzed side moves like a sliding
Examination curtain to the healthy side). In cases of submucous cleft
The examination begins by asking the patient to open palate, in addition to bifid uvula, a notch can be palpated
the mouth widely. Tongue depressor is used to examine in the midline of the posterior part of hard palate.
tonsillolingual sulcus, and to express contents of tonsillar Base of tongue: Posterior one-third of tongue is best exam-
ined by indirect laryngoscopy and finger palpation. It lies
Box 2: Oropharyngeal symptoms and their causes between the V-shaped row of circumvallate papillae and
the valleculae. Valleculae are two shallow depressions that
•• Sore throat and/or odynophagia (painful swallowing): lie between the base of tongue and the epiglottis.
Tonsillitis, pharyngitis, aphthous ulcers, abscesses Palpation: Palpation of oropharynx including base of
(peritonsillar, parapharyngeal, or retropharyngeal) and tongue is very important, as it helps in locating the infil-
lingual tonsillitis trative growth and its extension which is usually missed
during inspection. If the patient fails to relax, and does
•• Dysphagia (difficulty in swallowing): Tonsillar not cooperate even after 4% xylocaine spray, palpa-
enlargements, benign or malignant tumors of tonsils, tion must be conducted under general anesthesia. The
base of tongue, posterior pharyngeal wall and examiner must insert his/her finger in patient’s cheek
parapharyngeal region (especially in children) between the upper and lower
teeth to prevent biting on the examiner’s finger.
•• Nasal regurgitation of fluid: Paralysis of soft palate, cleft
palate, palatal perforation Laryngopharynx
For the evaluation (Symptoms and examination) of
•• Change in voice: Hypernasality (paralysis of palate), laryngopharynx, kindly see the chapter Laryngeal Symptoms
muffled or hot potato voice (space occupying lesions of and Examination in the section of larynx, trachea and
the oropharynx) bronchus.
•• Referred earache: Ulcers of the base of tongue, tonsil, Evaluation of Esophagus
pillars and palate
The symptoms of heartburn, dysphagia and odynophagia
•• Snoring or sleep apnea syndrome: Large tonsils and almost always suggest a primary esophageal disease.
tongue Heartburn (Pyrosis): This is sensation of substernal burning
•• Halitosis (bad smell from the mouth): Infected tonsils, that often radiates to the neck. It is highly indicative of
malignant tumors. gastroesophageal reflux disease (GERD). It is the reflux
of acidic (rarely alkali) material into the esophagus, and
discussed in detail in chapter Disorders of Esophagus.
Odynophagia: It is sharp retrosternal pain on swallowing
indicative of esophagitis due to candida, herpes viruses,
Cytomegalovirus (CMV), especially in immunocompromised
patients.The traumatic causes include caustic ingestions and
pill-induced ulcers (see chapter Disorders of Esophagus).
Dysphagia: The difficulty in swallowing is discussed in detail
in other section of this chapter.
418 Box 3: Findings of oropharyngeal examination and their causes
Section 5 w Pharynx and Esophagus •• Tonsils: Present/absent
–– Size: Large and obstructive; small or embedded
–– Symmetry: Unilateral or bilateral enlargement
–– Crypts: White or yellow spots at the openings (follicular tonsillitis); white excrescences which are not easily wiped off
(keratosis); expression of cheesy material (normal) or frank pus (septic tonsil)
–– Membrane: Membranous tonsillitis (diphtheria and Vincent’s angina)
–– Ulcer: Malignant, aphthous, Vincent’s angina, tuberculosis, ulcerating tonsillolith
–– Mass: Cystic (retention cyst), pedunculated or sessile solid mass (papilloma, fibroma), proliferative growth (cancer)
–– Bulge: Peritonsillitis and abscess, parapharyngeal abscess and tumor
–– Palpation: Hard (malignancy or tonsillolith), pulsation (internal carotid artery aneurysm), and bony (an elongated styloid
process)
–– Tonsillar pillars: Congestion, ulcer, proliferative growth
•• Soft palate: Redness, bulge or swelling (peritonsillitis), fibrous band (submucous fibrosis), vesicles, notch in the midline on
posterior part of hard palate (submucous cleft palate), paralysis, ulcers/growths (benign or malignant)
–– Uvula: Edematous, displaced to the opposite side (peritonsillar abscess, palatal palsy), bifid uvula, “curtain effect”
(paralysis of posterior pharyngeal wall)
•• Posterior pharyngeal wall: Lymphoid nodules (granular pharyngitis), post nasal purulent drip (chronic sinusitis), thin glazed
mucosa and crusting (atrophic pharyngitis), ulcers/growths (benign or malignant)
•• Base of tongue and valleculae: (Indirect laryngoscopy and palpation): Color of mucosa (normal or congested); prominent
veins, varicosities at the base of tongue or lingual thyroid, ulceration (malignancy, tuberculosis or syphilis), solid swelling
(lingual thyroid, lymphoma, carcinoma base of tongue), cystic swelling (vallecular cyst, dermoid or thyroglossal cyst)
BARIUM ESOPHAGOGRAPHY (Figs 2 and 3) Indications and Findings (Figs 4 to 6):
1. Malignant lesions: They show irregular narrowing of
Barium evaluation is gold standard for swallowing disorders lumen along with mucosal destruction, ulceration and
and esophageal function. It allows evaluation of tongue shouldering. The length of tumor is important for its
movement, soft palate elevation, epiglottic tilt, laryngeal staging.
closure and peristalsis of pharyngoesophageal segment. 2. Benign strictures: Smooth narrowing (may be at
It differentiates between mechanical lesions and motility multiple sites) of a short or long part of esophagus.
disorders. 3. Cardiac achalasia (cardiospasm): Markedly dilated,
Contraindications: Barium swallow is not used when aspira- elongated, and tortuous esophagus (mega esophagus)
having fluid level in lumen.
tion is present or suspected. Other contraindications include
perforation of pharynx and esophagus.
Fig. 2: Normal barium swallow of upper esophagus Fig. 3: Normal barium swallow of lower esophagus
Source: Dr Swati Shah, Professor, Radiodiagnosis, GCRI Medi- Source: Dr Swati Shah, Professor Radiodiagnosis, GCRI Medi-
cal College, Ahmedabad cal College, Ahmedabad
419
Fig. 4: Barium swallow. Filling defect in left pyriform fossa Fig. 6: Barium swallow. Abrupt obstruction at mid-esophageal Chapter 38 w Pharyngeal Symptoms and Examination
Source: Dr Swati Shah, Professor, Radiodiagnosis, GCRI Medi- level
Source: Dr Swati Shah, Professor, Radiodiagnosis, GCRI Medi-
cal College, Ahmedabad cal College, Ahmedabad
Cineradiography
High resolution images are obtained at a low frame rate.
It provides better spatial resolution for mucosal detail, and
reveals much of the swallowing dynamics.
Video Esophagography
Oropharyngeal dysphagia is best evaluated with this
technique. Low-resolution images are obtained at a high
frame rate. It allows longer exposure with less radiation. It
evaluates equivocal filling defects. Peristalsis is evaluated
with single swallow.
Fig. 5: Barium swallow. Mucosal irregularity in lower third of es- Modified Barium Swallow
ophagus and esophageal-gastric junction This procedure, which is usually conducted by radiologist
Source: Dr Swati Shah, Professor, Radiodiagnosis, GCRI Medi- in conjunction with the speech pathologist, evaluates
cal College, Ahmedabad coordination of swallow reflex and cause, and severity of
laryngotracheal aspirations. The patient is given varying
4. Esophageal varices: Irregular filling defects (like a string thickness of barium suspension, which mimics different
of pearls) in lower portion of esophagus. food consistencies.
Barium swallow vs Esophagoscopy: Many clinicians prefer Esophagogram
flexible endoscopy if they strongly suspect mechanical lesions. An esophagogram consists of three phases: Full column,
In motility disorders, barium swallow is done first as it provides air-contrast and mucosal relief.
more physiologic examination. Full column images: Single contrast study
Fluoroscopy Barium: Thin suspension of barium.
In fluoroscopy, imaging intensifier projects emitted light Pharynx: Best examined in standing position, and
on television screen which allows continuous monitoring
of moving process such as barium swallow study. extended neck prevents jaw from obscuring pharynx.
Esophagus: Patient is in prone oblique position, and
drinks barium from a straw. It evaluates esophageal
peristalsis and contour abnormalities. Rapid swallows
followed by Valsalva’s maneuver dilate the esophagus,
and helps in identifying contour defects.
Air contrast images: Double contrast study
Patient is upright, and slightly left anterior oblique.
420 Swallowing of an effervescent agent (for distending Extraesophageal symptoms: When atypical (extraesoph-
esophageal lumen) precedes swallowing of thick barium ageal) symptoms (chest pain, asthma, cough, hoarse-
Section 5 w Pharynx and Esophagus suspension. ness and sore throat) do not respond to PPI therapy.
Barium coats mucosal surface, and provides its exquisite ESOPHAGOSCOPY
detail. See chapter Endoscopies.
It can evaluate small mucosal tumors, and irregularities. DYSPHAGIA
Pharynx can be distended with phonation and modified
Dysphagia refers to difficulty in swallowing. It can be divided
Valsalva’s maneuver. into two types: oropharyngeal (difficulty in transferring food
Mucosal relief images: bolus from oropharynx to upper esophagus) and esophageal
(difficulty in transporting bolus through the body of
Thick barium suspension without effervescent agent. esophagus).
Good for distal esophagus, gastroesophageal junction, Oropharyngeal dysphagia: It is characterized by coughing,
and esophageal varices. choking and regurgitation immediately after initiation of swal-
Concluding images: lowing. Dysphagia is more with liquid than soft foods. It may
be associated with dysphonia, dysarthria, or other neurological
Valsalva and modified Valsalva’s maneuvers after features.The cause may be neurological, muscular, motility or
esophageal clearance should be done to see the gastro- structural disorders.
esophageal reflux. Neurological: Brainstem lesions (pseudobulbar palsy),
Oral Contrast Agents multiple sclerosis, or myasthenia gravis.
Barium suspension: Contraindicated in perforation of Muscular: Myopathies and hypothyroidism.
Motility: UES dysfunction.
pharynx and esophagus. Structural: Malignancy, surgery and Zenker’s diver-
Water-soluble contrast agents used in contrast CT: They are
ticulum.
Ionic contrast agents: Aspiration can lead to pneumo- Esophageal dysphagia: It may occur due to mechanical
nitis and pulmonary edema. Chances of allergic reac-
tions and airway compromise are more. obstruction or motility disorders.
Mechanical obstruction: The dysphagia is primarily for
Nonionic contrast agents: Safer but expensive.
Oil-based contrast agents: No more in use. solids, and is usually continuous and predictable. In
progressive lesions, dysphagia worsens with the prog-
ESOPHAGEAL MANOMETRY ress of the lesion. Some of the common causes include:
A small pressure-sensing catheter assembly is passed into –– Malignancy: Progressive dysphagia in elderly
esophagus through nose. It performs manometric study
of upper esophageal sphincter (UES), lower esophageal people.
sphincter (LES) and esophageal body. –– Peptic stricture: Chronic heartburn and progressive
Indications dysphagia.
To know the exact location of LES for placing a pH probe. –– Schatzki’s ring: Intermittent dysphagia which is not
To study peristaltic function of esophageal body before
progressive.
antireflux surgery. Motility disorders: The dysphagia is for both solids and
To confirm the diagnosis of esophageal motility disorders
liquids. It is episodic, unpredictable and non-progres-
(achalasia or diffuse esophageal spasm) suggested by sive. Some of the common causes include:
endoscopy or barium swallow. –– Achalasia: Progressive dysphagia.
–– Diffuse esophageal spasm (DES): Chest pain and
AMBULATORY 24-HOURS ESOPHAGEAL pH
RECORDING intermittent non-progressive dysphagia.
A small pH probe is passed nasally and placed 5 cm above –– Scleroderma: Dysphagia associated with chronic
LES. It is attached to a portable pH device that continuously
record pH for 24 hours. The pH recording tells about the heartburn and Raynaud’s phenomenon.
amount of acid esophageal reflux.The temporal correlations
between symptoms and reflux can be established. Odynophagia
It is sharp substernal pain on swallowing, and reflects
Indications severe erosive disease. The common causes include:
It is the best way for documenting acid reflux. It is indicated Infectious esophagitis due to candida, herpes viruses and
in GERD only in the following situations:
Preoperative: Before antireflux surgery when endoscopy is cytomegalovirus.
Corrosive injury due to caustic ingestion.
normal. Pill-induced esophagitis.
Proton pump inhibitor failures: Symptoms are not responding
Causes
to proton pump inhibitor (PPI) therapy, and endoscopy is The cause of dysphagia may lie in oral cavity, pharynx or
normal. esophagus (Box 4).
Box 4: Causes of dysphagia 421
• Oral Causes: They include disorders of following functions and structures:
Chapter 38 w Pharyngeal Symptoms and Examination
–– Chewing: Trismus, fractures of mandible, neoplasms of the upper or lower jaw, and temporomandibular joints disorders
–– Lubrication: Causes of xerostomia such as radiotherapy and Mikulicz disease
–– Tongue: Paralysis, painful ulcers, tumors, abscess and total glossectomy
–– Palate: Cleft palate and oronasal fistula
–– Buccal cavity and floor of mouth: Ulcers and Ludwig’s angina
• Pharyngeal Causes
–– Tumors: Tonsil, soft palate, pharynx, base of tongue, supraglottic larynx, or even obstructive hypertrophic tonsils
–– Inflammatory: Acute tonsillitis, peritonsillar abscess, retropharyngeal abscess, parapharyngeal abscess, acute epiglottitis,
edema of larynx
–– Spasmodic: Tetanus and rabies
–– Paralytic: Palatal palsy, which present with nasal regurgitation, may be caused by diphtheria, bulbar palsy, or cerebrovascular
accidents. Lesions of vagus and bilateral superior laryngeal nerves can lead to aspiration
• Esophageal Causes: The lesions may lie in the lumen, on the wall, or outside the wall of esophagus
–– Lumen obstruction: Atresia, foreign body, strictures, and benign or malignant tumors
–– Mucosal inflammation: Acute or chronic esophagitis
–– Motility disorders:
◊ Hypomotility: Achalasia, scleroderma, and amyotrophic lateral sclerosis
◊ Hypermotility: Cricopharyngeal spasm and diffuse esophageal spasm
–– External pressure:
◊ Hypopharyngeal diverticulum
◊ Hiatus hernia
◊ Cervical spines: Osteophytes
◊ Thyroid: Enlargement, tumors, and thyroiditis
◊ Mediastinal: tumor, lymph node enlargement, aortic aneurysm, cardiac enlargement
◊ Vascular rings: Dysphagia lusoria (Fig. 7)
Intermittent: Spasms or spasmodic episodes over an organic
lesion.
Liquids/solids: More with liquids (paralytic lesions), more
with solids, and progressing to liquids (malignancy).
Intolerance to acid food and fruit juices: Ulcerative lesions.
Associated complaints:
Regurgitation and heartburn: Hiatus hernia.
Regurgitation of undigested food in lying down and
coughing in night: Hypopharyngeal diverticulum.
Nasal regurgitation: Palatal paralysis.
Aspiration into lungs: Laryngeal paralysis.
Fig. 7: Pressure on thoracic esophagus from abnormal great Physical Examination
vessels as seen from behind. Dysphagia lusoria: (A) Double The physical examination should include oral cavity,
aorta; (B) Abnormal right subclavian artery oropharynx, hypopharynx, larynx, neck, chest and nervous
system including cranial nerves. The lesions of oral cavity
Evaluation and pharynx can be seen during physical examination
whereas esophageal causes require investigations such as
History barium swallow and esophagoscopy.
Sudden onset: Foreign body or impaction of food on a stric-
Investigations
ture or malignancy, and neurological lesions. Upper endoscopy, barium swallow, manometry and pH
Gradually progressive: Malignancy (short history with weight recording are the mainstay of dysphagia evaluation.
Hemogram: Iron deficiency anemia in Plummer-Vinson
loss) and peptic strictures (long history with heartburn).
Chronic, continuous and not progressive: Stricture. syndrome.
422 X-ray chest: For advanced esophageal lesions, cardiovas- Barium swallow: For malignancy, cardiac achalasia, strictures,
cular, pulmonary and mediastinal diseases or pneumome- diverticulum, hiatus hernia or esophageal spasms.
Section 5 w Pharynx and Esophagus diastinum.
Cineradiography: For motility disorders of esophageal wall
X-ray neck lateral and frontal projections: For cervical osteo- or sphincters.
phytes, lesions of post-cricoid or retropharyngeal region.
a. Useful in children. Ultrasound: Transesophageal echosonography can evaluate
b. Shows radiopaque foreign bodies. the depth of malignant ulcer, which helps in staging the
c. Saying“e”during exposure brings the tongue anterior, disease.
and shows oropharynx better.
d. Blowing through closed mouth distends hypo- Manometry and pH studies: For motility disorders, gastro-
pharynx. esophageal reflux and esophageal spasm (spontaneous
or acid induced). A pressure transducer along with a pH
Computed radiography and digital radiography: In this film- electrode and an open-tipped catheter are introduced into
less technique, image is captured on an array of digital the esophagus. They measure the pressures of esophageal
elements, and is read directly into a computer. wall and sphincters. Gastroesophageal reflux disease is
Advantages: measured by pH electrode, which also measures the effec-
Soft tissue differences: It can emphasize subtle soft tiveness of esophagus to clear the acid load.
tissue differences even if the image is suboptimally
exposed. Esophagoscopy (flexible or rigid): For direct examination of
Invert image: Radiodense elements appear whiter than esophageal mucosa and biopsy.
radiolucent elements on traditional films but computer
technology can invert the image and some aspects of Associated investigations: They vary from case to case such
anatomy, and pathology can be visualized better. as bronchoscopy for bronchial carcinoma, cardiac cath-
eterization for vascular anomalies, and thyroid scan for
malignant thyroid.
Clinical Highlight
1. Dysphagia lusoria: This dysphagia is caused by the compression of esophagus by an abnormal right subclavian artery,
which abnormally arise directly from the aorta and passes anterior or posterior to esophagus.
FURTHER READING
1. Ghosh SK, Saha J, Chandra S, et al. Pleomorphic adenoma of the base of the tongue: A case report. India J Otolaryngol Head Neck
Surg. 2011;63:S113-4.
2. Rajeshwari A, Somayaji G, Shetty D. A rare cause of dysphagia: A case report. India J Otolaryngol Head Neck Surg. 2011;63:S83-4.
3. Roy M, Rupa V, Deepthi AN, et al. Unusual cystic hypopharyngeal mass in a child with obstructive. India J Otolaryngol Head Neck
Surg. 2011;63:S41-3.
4. Sethi A, Sethi D, Bansal R. True hamartoma of the tonsil. India J Otolaryngol Head Neck Surg. 2011;63:S99-101.
5. Sinha V, Ray S. The relative sensitivity of barium swallow examination. Indian J Otolaryngol Head Neck Surg. 2002;54:313-4.
39 Pharyngitis and
Adenotonsillar Disease
Doing good to others is virtue; injuring others is sin. Strength and manliness are virtue; weakness and cowardice are sins.
Independence is virtue; dependence is sin. Loving others is virtue; hating others is sin. Faith in God and in one’s own self is virtue;
doubt is sin. Knowledge of oneness is virtue; seeing diversity is sin.
— Swami Vivekananda
Points of Focus ¯¯Tonsillar concretions/Tonsilloliths
¯¯INTRODUCTION ¯¯Intratonsillar abscess
¯¯Pharyngitis ¯¯Tonsillar cyst
¯¯Keratosis pharyngitis
Irritative ¯¯Diseases of lingual tonsils
Bacterial and Viral ¯¯Chronic adenotonsillar hypertrophy
¯¯Adenoid facies and Craniofacial growth
¯¯Infectious mononucleosis
¯¯Streptococcal tonsillitis-pharyngitis abnormalities
¯¯Obstructive sleep apnea
membranous pharyngitis-tonsillits ¯¯Clinical Highlights
white patches on tonsils
¯¯Faucial Diphtheria
INTRODUCTION Irritative Pharyngitis
Infections of pharynx, tonsil and adenoids account for a signifi- The causes of this common condition include:
cant proportion of childhood illnesses. They often lead to two Postnasal drip
of the most common pediatric surgeries—tonsillectomy and Laryngopharyngeal reflux
adenoidectomy. The predominant symptom of oropharyngeal Occupational and environmental exposures.
infection is sore throat, which is one of the most common chief
complaints to physicians. Bacterial Pharyngitis
In children, bacterial pharyngitis accounts for 30–40% of
PHARYNGITIS
Pharyngitis refers to inflammation of the pharynx mainly cases while in adults, it accounts for only 5–10%.
oropharynx. Acute catarrhal or superficial tonsillitis is a part of Most cases of bacterial pharyngitis are caused by group A
generalized pharyngitis, and is mostly seen in viral infections.
In parenchymatous tonsillitis, which affects tonsil substance, b-hemolytic Streptococcus (GABHS) pyogenes.
tonsil is uniformly enlarged and red. Pharyngitis is common in Hoarseness and cough are not suggestive of pharyngitis.
adults while tonsillitis is mainly a disease of children. Majority It is important to confirm the diagnosis of GABHS because
of pharyngeal infections in adults are viral. The Streptococcus
pyogenes only accounts for 5–10% in adults. majority of acute pharyngitis cases do not have strepto-
coccal infection.
See the section streptococcal tonsillitis-pharyngitis.
424 Viral Pharyngitis Ampicillin causes skin rash in this condition and should be
Coxsackie virus infections avoided.
Section 5 w Pharynx and Esophagus Management of upper airway obstruction: Airway obstruc-
Herpangina: It mostly affects children. Child pres- tion can occur due to significantly enlarged tonsils. It is
ents with fever, sore throat, and vesicular eruption managed with:
surrounded by a zone of erythema on the soft palate Nasopharyngeal airway
and pillars (See chapter: Oral Mucosal Lesions). High dose steroids
Tonsillectomy or tracheostomy.
Acute lymphonodular pharyngitis: It presents with fever,
malaise and sore throat. White yellow, solid nodules on Infectious mononucleosis: Amoxicillin or ampicillin can cause
the posterior pharyngeal wall may be seen on exami- a salmon-colored rash.
nation.
Streptococcal Tonsillitis-Pharyngiti
Cytomegalovirus: It affects immunosuppressed transplant In acute follicular tonsillitis, infection spreads into the crypts
patients. The infection mimics infectious mononucleosis which become filled with purulent material. The openings of
but heterophil antibody test is negative. crypts present yellowish spots of pus which may coalesce, and
form a membrane on the surface of tonsil (acute membranous
Pharyngoconjunctival fever: It is caused by adenovirus, and tonsillitis).
presents with sore throat, fever and conjunctivitis. Pain in
abdomen mimics appendicitis. Etiology
GABHS is a precursor of two serious conditions acute rheu-
Measles: It is characterized by Koplik’s spots (white spots
surrounded by red areola) on the buccal mucosa opposite matic fever and poststreptococcal glomerulonephritis. It
of the molar teeth 3–4 days before the rash. is the most common cause of acute bacterial tonsillitis-
pharyngitis. Epidemic forms are seen in recruit camps and
Common cold (Rhinovirus, Corona virus, Parainfluenza virus): daycare facilities. GABHS are Gram-positive cocci that grow
It may affect tonsils and pharynx, and present with sore in chain.
throat, dysphagia and fever. Tonsils may be enlarged but Natural reservoir: Skin, nasopharynx and orophar ynx.
there is no exudate. Spread: Mostly through aerosolized microdroplets; less
Herpes simplex virus: It may cause exudative or nonexudative commonly by direct contact, and rarely through inges-
pharyngitis, which may be associated with gingivostoma- tion of contaminated non-pasteurized milk or food.
titis (See chapter: Oral Mucosal Lesions). Seasons: Autumn and winter.
Non-group A b-hemolytic streptococcal infection is clinically
Treatment similar to GABHS. It is comparatively less common.
Treatment of viral infection is nonspecific and symptomatic. The other bacteria may primarily infect the tonsil or may be
Antibiotics are used for secondary bacterial colonization secondary to a viral infection and mimic GABHS infection.
They include staphylococci, pneumococci and H. influenzae.
(Gram-negative and S. aureus), which increases by about
50% in these viral diseases. Clinical Features
The disease often affects school going children (peak 5–6 years),
Infectious mononucleosis but may affect infants and individuals above 50 years of age.
Infectious mononucleosis is caused by Epstein-Barr virus. Symptoms
Throat pain: Dry throat, fullness in throat or sore throat.
Clinical Features Dysphagia: Difficulty in swallowing or odynophagia.
Often affects older children and young adults Fever: Temperatures 38–40°C may be associated with chills
Fever, sore throat, exudative pharyngitis
Both tonsils are enlarged, congested and covered with and rigors. The child may present as a case of pyrexia of
unknown origin.
membrane Earache: It may be either referred, or due to acute otitis
Marked local discomfort. media.
Lymphadenopathy: Lymph nodes enlarged in the posterior Constitutional symptoms: Headache, limb and back pain,
malaise and constipation.
triangle of neck. Abdominal pain: It is due to mesenteric lymphadenitis, and
Hepatosplenomegaly. simulates acute appendicitis.
Physical Findings
Diagnosis Tongue: Dry and coated tongue.
Characteristic feature: Petechiae at the junction of hard and Breath: Fetid breath (halitosis).
Oropharynx:
soft palate. Hyperemia of pillars, soft palate and uvula.
CBC: Fifty percent lymphocytes, of which 10% are atypical. Tonsils red and swollen with yellowish spots of pus at
White cell count normal in first week and rises in second the opening of crypts (acute follicular tonsillitis) which
week.
Serological tests: Monospot and Paul Bunnell or Ox-cell
hemolysis test shows high titers of heterophil antibody.
Treatment
Symptomatic and recovery may take weeks.
Antibiotics: No role except in secondary bacterial infection.
may coalesce, and form a membrane on the surface of Cervical abscess: Suppuration of jugulodigastric lymph 425
tonsil (acute membranous tonsillitis). This membrane nodes.
can be easily wiped away with a swab. The enlarged Chapter 39 w Pharyngitis and Adenotonsillar Disease
tonsils may meet in midline. Differential Diagnosis of Membranous
Edema of the uvula and soft palate may be present. Pharyngitis-Tonsillitis
Lymph nodes: Enlarged and tender jugulodigastric lymph In membranous tonsillitis an exudative membrane forms over
nodes. the medial surface of the tonsils. It occurs due to pyogenic
organisms.
Diagnosis Agranulocytosis:
Sore throat and fever with cervical adenopathy and pharynx
with exudative covering are highly suggestive of Streptococcus Ulcerative necrotic lesions in the oropharynx.
pyogenes. Patient looks very ill.
Rapid strep tests: Latex agglutination or enzyme-linked Diagnosis:
immunosorbent assay (ELISA) methods extract antigen –– Total leukocyte count: 50–2000/cumm.
(group-A streptococcal) from a swab. It is highly specific –– Polymorph neutrophil 5% or less.
(95%), but less sensitive (60–100%) than culture. Leukemia: In children, acute lymphoblastic leukemia is more
Throat culture: Swab the posterior pharynx and tonsillar common (75%) than acute or chronic myelogenous (25%)
area when body temperature is greater than 38.3°C or when leukemia. In adults, 80% are nonlymphocytic, and 20% are
patient presents only with sore throat, or when rapid strep acute lymphocytic leukemia.
test is negative in strongly suspected cases. TLC: Greater than 100,000/cumm.
Progressive anemia.
Treatment Bone marrow examination: Blasts cells are seen.
General: Bed rest and plenty of fluids. Aphthous ulcers: Small/large, single/multiple painful ulcers
Symptomatic: Analgesics and antipyretics such as aspirin on any part of oral cavity or oropharynx. Solitary big
ulcer may involve the tonsil and pillars. (See chapter: Oral
or paracetamol. Mucosal Lesions).
Specific: Antibiotics for 7–10 days reduces the chances Malignancy tonsil: (See Chapter: Tumors of Oropharynx).
Traumatic ulcer: Any injury to oropharynx. It may be accidental
of suppurative complications and acute rheumatic fever, due to a tooth brush, a pencil or finger. It heals by formation
but not poststreptococcal glomerulonephritis. of a membrane which appears within 24 hours.
Penicillin or amoxicillin is the drug of choice. If there is Diphtheria: See following section and Table 1.
Infectious mononucleosis: See other section.
no response then suspect beta-lactamase producing Vincent’s angina: (See chapter: Oral Mucosal Lesions).
organisms and anaerobes, and start Causative organism: Fusiform bacilli and spirochetes.
–– Amoxicillin + clavulanic acid or Clinical Features: It has insidious onset with mild fever
–– Clindamycin or and discomfort in throat. It presents with membrane,
–– Erythromycin + metronidazole which usually involves one tonsil.This pseudomembrane
Asymptomatic carriers: They usually do not need any treat- can be easily removed, and reveal an irregular ulcer.
ment except when: Diagnosis: Throat swab shows the causative organisms.
Family member is having rheumatic fever.
Family members are getting recurrent streptococcal Differential Diagnoses of White Patches
infection. on Tonsils
In addition to the above-mentioned causes of membranous
Group A beta-hemolytic streptococci: It is the most common pharyngitis-tonsillitis, certain conditions (Box 1), most of which
cause of acute tonsillitis and can also result in rheumatic fever are described in the sections of this chapter, can present with
and poststreptococcal glomerulonephritis. white lesions on the tonsils.
Complications Faucial Diphtheria
Scarlet fever The increasing coverage of child population by diphtheria
Rheumatic fever immunization [combined (DPT, DT, dT) and single vaccines]
Acute glomerulonephritis has significantly reduced the incidence of diphtheria. The
Acute otitis media: It may coincide with recurrent tonsillitis. disease was quite common and feared of. It is now fortu-
Subacute bacterial endocarditis (SABE): Acute tonsillitis nately seen uncommonly. However, it should be kept in
mind whenever any membrane is seen on the tonsils of a
in cases of valvular heart disease can cause SABE, which child (Table 1).
is usually due to streptococcus viridans. Causative organisms: Gram-positive bacilli, Coryneba cterium
Chronic/Recurrent tonsillitis due to incomplete resolution
of tonsil infection, which may persist in lymphoid follicles diphtheriae.
of the tonsil like microabscesses. Spread: It spreads by droplet infection. Diphtheria carriers
Peritonsillar abscess
Parapharyngeal abscess harbor organisms in their throat, and have no symptoms.
Retropharyngeal space infection Incubation period: 2–6 days.
426 Box 1: Differential diagnoses of white patches on tonsils Urine may show albumin.
• Trauma: Foreign body induced ulcer and infection, thermal Smear and culture of throat swab will reveal Corynebacterium
Section 5 w Pharynx and Esophagus
injuries (hot meal and chemicals) and radiotherapy diphtheriae.
• Bacterial infections: Acute tonsillitis, diphtheria, Vincent’s
Complications
angina Diphtheria exotoxin is toxic to heart and nerves.
• Fungal infections: Candidiasis Heart: Myocarditis, cardiac arrhythmia and acute circula-
• Viral infections: Herpes, infectious mononucleosis
• Blood dyscrasias tory failure.
• Chronic infections: Tuberculosis (painful multiple white Neurological: Paralysis of palate, diaphragm and ocular muscles.
Larynx: Airway obstruction.
patches) and syphilis
• Benign tumors: Papilloma Treatment
• Malignant: Irregular white patch with everted margin and Antidiphtheric serum: Antidiphtheric serum (ADS) is started
induration (carcinoma), smooth nonulcerated swelling with immediately on clinical suspicion to neutralize the free
induration (lymphoepithelioma) diphtheria exotoxin. Dose depends on the site, duration
• Tonsillar cyst (Congenital or acquired): Yellowish white and severity of disease.
• Tonsillar keratosis: Whitish horny outgrowths 20,000 to 40,000 units: History of less than 48 hours, or
• Tonsillolith: Hard whitish lesion
• Aphthous ulcer: Intensely painful membrane is limited to tonsils only.
80,000 to 120,000 units: History of more than 48 hours,
Clinical Features
Children are affected more. or membrane extends beyond tonsils.
Diphtheria has slow onset of local discomfort. Mode of administration: Intravenous infusion in saline
Fever seldom rises above 38°C.
The dirty gray tenacious membrane extends beyond the in about 60 minutes.
Sensitivity test: Horse serum is tested by conjunctival or
tonsils on to the soft palate and posterior pharyngeal wall
and after removal, leaves a raw bleeding surface. intracutaneous test with diluted antitoxin. Adrenaline
Larynx and nasal cavity can also be affected. must be handy for any hypersensitivity reaction.
Cervical lymph nodes (jugulodigastric) get enlarged and Desensitization: Desensitization is required if patient is
tender, and may present as “bull-neck” appearance. hypersensitive to ADS.
The child looks ill and toxemic. Antibiotics:
Benzyl penicillin 600 mg 6 hourly for 7 days.
Diagnosis Erythromycin 500 mg 6 hourly orally in penicillin sensi-
Diphtheria is usually a clinical diagnosis and in cases of doubt, tive individuals.
the child should be treated on the line of diphtheria without
wasting much time. Tonsillar Concretions/Tonsilloliths
Tonsillolith (calculus of the tonsil) may be seen in chronic
tonsillitis. The blocked tonsillar crypt causes retention of debris,
which consists of inorganic salts of calcium and magnesium
(formation of stone).
Table 1 Distinguishing features of acute follicular tonsillitis and diphtheria
Features Acute follicular tonsillitis Diphtheria
Past history Recurrent sore throat with fever Contact with diphtheria patient
Diphtheria vaccination Taken Not taken
Age No age bar Children
Onset Acute Insidious
Throat pain Severe Mild
Fever High grade Low grade
Hoarseness of voice and respiratory Never Present in advanced disease
distress
Neck bull due to cervical Absent not uncommon
lymphadenopathy
Pulse rate In proportion to fever Out of proportion to fever and weak
Toxemia Absent Present in advanced disease
Tonsillar membrane Limited to tonsil and easily May extend adjacent structures, and difficult to
removed remove, and leaves raw bleeding area
Throat swab Streptococci Corynebacterium diphtheriae
Urine No albumin Albumin often present
First line of treatment Antibiotics Antidiphtheric serum
Mortality Nil High
Clinical Features Clinical Features 427
The affected crypt gradually enlarges, and may ulcerate on Discomfort on swallowing
Feeling of lump in the throat Chapter 39 w Pharyngitis and Adenotonsillar Disease
medial surface of tonsil. Dry cough
Retained material may have bacterial growth and then Thick voice
Lingual tonsil are enlarged, and congested or studded with
present with halitosis and sore throat.
Whitish foul-tasting and foul-smelling cheesy material can follicles
Cervical lymph nodes are enlarged
be expressed from tonsils.
Tonsilloliths are usually seen in adults. Patient presents Treatment
Antibiotics
with local discomfort or foreign body sensation. They are Diathermy coagulation or excision of lingual tonsils (by
diagnosed by palpation or probing.
conventional or laser surgery).
Treatment
Lingual tonsillar abscess
Conservative: Expression of concretions/cheesy material and Clinical Features:
chemical cauterization of crypts with topical silver nitrate
application. Severe unilateral dysphagia and excessive salivation.
Pain in the tongue
Tonsillectomy: In cases of persistent pain, halitosis, or foreign Enlarged and tender jugulodigastric nodes.
body sensation. Complications: Laryngeal edema.
Treatment: Antibiotics, analgesics, proper hydration and
Intratonsillar abscess incision and drainage of the abscess.
Accumulation of pus within the blocked tonsillar crypt can
occur in cases of acute follicular tonsillitis. CHRONIC ADENOTONSILLAR
Clinical Features HYPERTROPHY
Adenotonsillar hypertrophy (Fig. 1) can cause obstructive sleep
Marked local pain and dysphagia. apnea (OSA) and affect craniofacial growth and microbiologic
Tonsil swollen and red. flora of tonsils and adenoids (chronic adenotonsillar hyper-
Treatment trophy).
Antibiotics
Drainage of the abscess
Tonsillectomy
Tonsillar cyst Etiology
Physiological: In children, there occur physiological enlarge-
Blocked tonsillar crypt may present as a yellowish swelling
over the tonsil. ment of adenoids and tonsils (associated with generalized
Usually they are asymptomatic. lymphoid hyperplasia) in the first to the fourth year of life
If symptomatic, it can be drained. due to increased immunologic activity.
Infection: b-lactamase producer pathogenic bacteria.
Keratosis Pharyngitis Recurrent rhinitis and sinusitis.
White or yellowish dots or horny excrescences on the surface
of tonsils, pharyngeal wall or lingual tonsils characterize this
benign condition. These excrescences are firmly adherent
and cannot be wiped off. They are the result of hypertrophy
and keratinization of epithelium.
Patient does not have features of acute follicular tonsillitis
such as sore throat, fever, cervical nodes and exudates.
Treatment
The spontaneous regression does occur so, no specific
treatment is required.
The concerned patients need reassurance.
Diseases of Lingual Tonsils Fig. 1: Kissing tonsils
Hypertrophy, infection or abscess can occur in lingual tonsil.
Compensatory hypertrophy of lymphoid tissue may occur in
response to repeated infections especially in tonsillectomy
patients.
428 Allergy of upper respiratory tract. Diagnostic Assessment of Tonsils and Adenoids
Irritation: Second hand smoke exposure. Clinical: Confirm the features of adenotonsillar hypertrophy
Section 5 w Pharynx and Esophagus
Clinical Features mentioned above.
The size of the adenoid mass (relative to the available space in Postnasal mirror examination: An adenoid mass can be seen.
the nasopharynx) and infection are important in causing the X-ray soft tissue nasopharynx lateral view: Reveal size of
nasal, aural or general symptoms.
Nasal: adenoids, and extent of nasopharyngeal air space compro-
mise.
Nasal obstruction: Mouth breathing is one of the Rigid or flexible nasopharyngoscope under topical anesthesia:
commonest symptoms. It interferes with feeding or Shows details of the nasopharynx.
suckling (respiration and feeding cannot take place Nasal obstruction: Evaluate for other causes of nasal obstruc-
simultaneously). The child may fail to thrive. tion such as turbinate hypertrophy.
Nasal discharge: The choanal obstruction and asso- Assess for overt or submucous cleft of palate: See for bifid uvula
ciated chronic rhinosinusitis may present with wet and translucent line through the mid soft palate, and palpate for
bubbly nose. notching of posterior part of hard palate. It is important before
adenotonsillectomy.
Epistaxis: Not common. Acute adenoiditis may cause
epistaxis. Obstructive Sleep Apnea
In children, adenotonsillar hypertrophy is the most common
Rhinolalia clausa: Voice becomes toneless and loses cause of sleep apnea.
nasal quality.
Clinical Features
Ear: Eustachian tube obstruction and infection may result The sleep disturbances may have the following consequences:
in following features: Episodes of apnea
Conductive hearing loss and retracted tympanic Too much loud snoring
membrane. Chronic mouth breathing
Recurrent acute otitis media. Interrupted sleep with frequent awakening and nightmares
Chronic suppurative otitis media. Hypersomnolence
Serous otitis media. Poor school/work performance
Dysphagia
ADENOID FACIES AND CRANIOFACIAL Hyponasal speech (rhinolalia clausa)
GROWTH ABNORMALITIES Failure to thrive: OSA in children may disrupt growth
The characteristic facial appearance called“adenoid facies”and
craniofacial growth abnormalities are caused due to chronic hormone during REM sleep.
nasal obstruction and mouth breathing. The features, some of Enuresis: Children with secondary enuresis (develop later
which are reversed after adenotonsillectomy, include:
An elongated face in childhood) associated with significant airway obstruc-
Retrognathic mandible tion due to adenotonsillar hypertrophy usually respond to
Dull expression adenotonsillectomy. Primary enuresis, which is congeni-
Dark circles under the eyes tally present, does not respond to this surgery.
Open mouth Obesity: Like adults (classic obesity-related pickwickian
Pinched nose due to disuse atrophy of alae nasi syndrome), obesity is not a factor in pediatric OSA. It is due
Hitched up upper lip to adenotonsillar hypertrophy (see chapter Obstructive
Open bite, protrusive maxilla and buccal posterior crossbite Sleep Apnea).
Prominent and crowded upper teeth
High arched hard palate because of the absence of Diagnosis
Polysomnography: This expensive testing is not must in
moulding action of the tongue.
The children with adenotonsillar hypertrophy, which are pediatric OSA, which is associated with confirmed adeno-
considered for orthodontic procedures for malocclusion, should tonsillar hypertrophy. But it is required in children where
have an ENT evaluation. OSA is not associated with adenotonsillar hypertrophy.
Sleep sonography: Tape recording of night sleep patterns at
Airway Obstruction patient’s home reliably detects evidence of OSA. It is an easy
Excessive loud snoring at night and most economical method of diagnosing OSA.
Cor pulmonale: Chronic upper airway obstruction due to X-ray chest and ECG should be taken preoperatively.
chronic adenotonsillar hypertrophy leads to pulmonary Treatment
ventilation-perfusion abnormality and chronic alveolar Medical: Following measures may cure early disease without
hypoventilation. The chronic hypercapnia and hypoxia
result in respiratory acidemia, pulmonary artery vasocon- resort to surgery:
striction, and right ventricular dilation and then eventually Breathing exercises
cardiac failure.
Obstructive sleep apnea
Decongested, saline or steroid nasal drops Surgical: Adenotonsillectomy 429
Antihistaminics For indications, contraindications, preoperative
Antibiotics assessment, surgical techniques, postoperative care
Management of any associated nasal allergy. and complications see chapter: Adenotons illectomy.
Clinical Highlights Chapter 39 w Pharyngitis and Adenotonsillar Disease
1. Acute tonsillitis: Most common causative microorganism of acute tonsillitis is Streptococcus haemolyticus (Group A
beta-hemolytic Streptococcus pyogenes).
2. Pharyngoconjunctival fever: It occurs in epidemics and causes follicular conjunctivitis and acute pharyngitis with fever.
3. Herpangina: This self limiting infection of children causes sore throat and fever.
4. Infectious mononucleosis: The sore throat and fever is associated with generalized lymphadenopathy and splenomegaly.
Atypical lymphocytes are seen in peripheral smear.
5. Faucial diphtheria: It can cause palatal palsy.
6. Vincent’s angina: The clinical features include gingivitis, stomatitis and ulceration of the tonsils.
7. Gray white membrane on the tonsils: Some of the causes are infectious mononucleosis, streptococcal tonsillitis and
diphtheria.
8. Keratosis pharyngitis: Yellow spots over the tonsil are not easy to wipe off.
9. Adenoid face: In children with adenoid hyperplasia, facies show crowded teeth, high-arched palate, open mouth with
under slung lower jaw and underdeveloped/pinched nostrils.
10. Adenoid hypertrophy: Nasopharyngeal obstruction can cause sinusitis, serous otitis media, and cor pulmonale.
Management of adenoid hypertrophy with conductive hearing loss due to otitis media with effusion (OME) is adenoidectomy
with grommet insertion.
11. Rhinolalia clausa: The common causes include allergic rhinitis, adenoids and nasal polyps.
12. Cor pulmonale: It can occur in children with chronic obstruction of upper respiratory tract due to enlarged tonsils and
adenoids.
FURTHER READING
1. Batra K, Safaya A, Nair D, et al. Sore throat—a review of presentation and etiology. Indian J Otolaryngol Head Neck Surg. 2004;56:14-20.
2. Jain A. Peritonsillolith. Indian J Otolaryngol Head Neck Surg. 2003;55:263-4.
3. Jana U, Mukherjee S. Tuberculosis of tonsil—a rare site involvement. Indian J Otolaryngol Head Neck Surg. 2003;55:119-20.
4. Knotra S, Kanotra S, Paul J. A giant tonsillolith. Indian J Otolaryngol Head Neck Surg. 2008;60:277-80.
5. Kumar A, Gupta V, Chandra K, et al. Clinico bacteriological evaluation of surface and core microflora in chronic tonsillitis. Indian J
Otolaryngol Head Neck Surg. 2005;57:118-20.
6. Lecha A, Kurien M, Job A, et al. Chronic adenoid hypertrophy in children—is steroid nasal spray beneficial? Indian J Otolaryngol Head
Neck Surg. 2002;54:280-4.
7. Rehan HS. Pattern of drug utilization in acute tonsillitis in a teaching hospital in Nepal. Indian J Otolaryngol Head Neck Surg. 2003;55:176-9.
8. Subashini P, Ravikumar A, Ranjit MS, et al. Adenoid hypertrophy presenting with systemic hypertension. Indian J Otolaryngol Head
Neck Surg. 2007;59:73-5.
9. Wakode PT, Gawarle SH, Joshi SV, et al. Throat swab culture & sensitivity reports: an overview. Indian J Otolaryngol Head Neck Surg.
2003;55:76-80.
10. Reader’s Forum-28. How do you treat nonspecific pharyngitis with all its vague symptoms and anxiety amongst your patients? How
important is gastroesophageal reflux benign it’s cause? Indian J Otolaryngol Head Neck Surg. 2002;54:317-8.
40 Sleep apnea and Sleep-
disordered Breathing
Isn’t it man that makes money? Where did you ever hear of money making man? If you can make your thoughts and words perfectly
at one, if you can, I say, make yourself one in speech and action, money will pour in at your feet of itself, like water.
— Swami Vivekananda
Points of Focus Multiple sleep lateney test
¯¯Introduction ¯¯Severity of osa
Classifications ¯¯Complications of osa
¯¯Nonsurgical Treatment
¯¯Pathophysiology of obstructive sleep
apnea Lifestyle modifications
Sleep patterns in OSA Nasal continuous positive airway pressure
Factors aggravating OSA Intraoral devices
¯¯Diagnosis And Evaluation of osa ¯¯Surgical Treatment of OSA
History Uvulopalatopharyngoplasty
Physical examination Other surgical procedures
Flexible nasopharyngolaryngoscopy
Radiography ¯¯Surgical Treatment of Snoring Without OSA
Polysomnography
Home sleep studies ¯¯Clinical Highlights
Introduction Classifications
Sleep-disordered breathing (SDB) is a type of intrinsic sleep Snoring: In this noisy breathing, a rough, rattling inspiratory
disorder (dyssomnia). It encompasses primary snoring, upper
airway resistance syndrome (UARS), obstructive sleep apnea noise is produced by vibration of pendulous soft palate, or
syndrome and obesity-hypoventilation syndrome (Pickwickian occasionally of vocal cords, during sleep.
syndrome). SDB (apnea-hypopnea index of 5 or more per hour Primary snoring: In these snorers, an apnea-hypopnea
of sleep) occurs in about 9% women and 24% men between the
ages of 30 and 60 years. Among the women SDB is more common index is less than 5 events per hour of sleep.
in postmenopausal age. About 70% SDB patients are obese. Upper airway resistance syndrome: These patients have
About 25% of adults snore and the prevalence rises with an apnea-hypopnea index of less than 5 events per hour
increasing age. About 60% of males over 60 years of age have of sleep but have an elevated arousal index (more than
snoring. Though snoring does indicate some obstruction in 5 times per hour).
upper airway most snorers have no obstructive sleep apnea Sleep apnea: It refers to intermittent cessation of breathing
(OSA). Although OSA patients are typically loud snorers, not for 10 seconds or longer during sleep. The airflow is usually
all people who snore have OSA. Snoring and OSA probably measured at the nose and lips. There are three classes of
represent a continuum of a similar pathology. There is difference sleep apnea: central, obstructive and mixed.
between the noise of snoring and stridor. Obstructive sleep apnea syndrome: In obstructive
sleep apnea syndrome (OSAS) transient upper airway
obstruction results in intermittent cessation of air flow or
breathing though there is normal respiratory effort. This OSA patients mainly have less deep sleep of Stage I and II. Due 431
is the most common type of sleep apnea and is managed to these restless sleep patterns, these patients are deprived of
by ENT surgeons. An apnea-hypopnea index is more than deep sleep and have daytime somnolence. So the OSA patients Chapter 40 w Sleep apnea and Sleep-disordered Breathing
5 events per hour of sleep. During the episodes, oxyhe- have quick onset of sleep and multiple arousals. The successful
moglobin desaturation becomes less than 90%. treatment of OSA results in increase in REM sleep.
Central sleep apnea: Intermittent failure in the respira-
tory drive centers in central nervous system (CNS) results Factors Aggravating OSA
in cessation in air flow or breathing. The phrenic nerve Certain factors are known to exacerbate OSA episodes. Most
and diaphragm become temporarily inactive.There is no snoring is not pathologic and may be prevented by life style
obstruction in upper respiratory tract. This class of sleep changes by managing factors mentioned in Box 1.
apnea is managed by neurologists and sleep specialists.
Mixed sleep apnea: This variant of OSA has compo- Diagnosis and evaluation of osa
nents of both central and obstructive sleep apnea.
Pickwickian syndrome: This syndrome is characterized by History
obesity and hypersomnolence. It was described by Charles Though not found totally reliable, history of sleep apnea is elic-
Dickens in The Pickwick Papers. In obese persons, weight ited from the spouse. The symptoms are listed in Box 2. Though
of neck, redundant soft palate and thick base of tongue not pathognomonic the typical symptoms are snoring, day time
contribute to OSA. somnolence, morning headache and restless sleep. Periods of
Stridor: A high-pitched, noisy respiration, like the blowing apnea result in frequent arousals at night. The neurobehavioral
of the wind is a sign of respiratory obstruction, especially symptoms affect school and work performance.
in the larynx or trachea. See chapter Laryngeal Symptoms
and Examination. Physical Examination
Congenital stridor: Crowing inspiration occurs at birth or ENT head and neck examination: Patients with OSA need
within the first few months of life. It may be without any
apparent cause or due to abnormally flaccid epiglottis complete ENT, head and neck examination and measurement
or arytenoids. of blood pressure, neck circumference and body mass index.
Expiratory stridor: A singing sound comes from semi- The common findings, which constitute even the etiological
approximated vocal folds offering resistance to the factors, are mentioned in Box 3. In children OSA is generally
escape of air. due to tonsil (Fig. 1) and adenoid hypertrophy. For pediatric
Inspiratory stridor: An inspiratory crowing sound occurs OSA see chapter Pharyngitis and Adenotonsillar Diseases.
due the pathology of epiglottis or larynx. Body mass index: The body weight in kilogram is divided by
the height in square meters.
Pathophysiology of OBSTRUCTIVE SLEEP Normal: 18.5 to 24.9
APNEA Over weight: 25 to 29
An obstruction at any level of upper respiratory tract (i.e. from nose Obesity: 30 to 34.9
to the true vocal cords) can result in OSA. During inspiration there Collar size: Neck circumference at the level of cricothyroid
occurs a negative pressure within upper respiratory tract. Muscle membrane should not exceed 42 cm in male and 37.5 cm
relaxation of whole body (including muscles of upper respiratory in females.
airway) occurs during the deeper stages of sleep (Stages III, IV and
REM).These two factors (muscle relaxation and negative pressure) Box 2: Symptoms of obstructive sleep apnea
results in collapse and obstruction of the airway in the patients, • Snoring
who have redundant tissue or narrow airway. Obstruction of airway
leads to oxyhemoglobin desaturation that results in arousal and –– Family members complain about patient’s loud snoring
brings the patient to a lighter level of sleep. The upper respiratory • Daytime somnolence
airway is established again with the loud snorting breathing. The
factors mentioned in Box 1 can cause or exacerbate OSA. –– Drowsiness at work
–– Fall asleep at work, while driving, or on telephone
Sleep Patterns in OSA • Morning headache and fatigue
During the deep stages of sleep (Stage III, IV and REM) most • Restless sleep
obstructive events occur as the muscles are most relaxed. So the –– Patient does not feel rested after night sleep
• Periods of apnea (cessation of breathing) resulting in frequent
Box 1: Factors aggravating OSA arousals at night
• Alcohol –– Sudden awakening and gasping for air
• Sedatives including antihistamines and cough suppressants • Decreased libido and impotence
• Allergic rhinitis • Indigestion and gastroesophageal reflux disease
• Upper respiratory infections (URI) • Hypertension
• Weigh gain • Decreased cognitive function including memory loss
• Supine position. • Personality changes, depression and psychosis
• Nocturnal headache, sweating, enuresis.
432 Box 3: Etiological findings on physical examination and skeletal obstruction in upper airway. Though limited
in patients with OSA by two dimensions this simple and cost-effective method
Section 5 w Pharynx and Esophagus measures posterior airway space and evaluates maxillary
• Nose: Deviated septum, hypertrophic turbinates, allergic and mandibular development.
rhinitis, nasal valve collapse, polyps/tumors
Polysomnography
• Oral cavity: Macroglossia, retrognathia, micrognathia, large This is the gold standard test in the evaluation of OSA. It differen-
mandibular tori tiates not only between snoring without OSA, OSA and central
sleep apnea but also identifies the severity of the apnea. This
• Oropharynx: Large tonsils, redundant or large soft palate, expensive test can be done in a sleep lab or in a patient’s home.
large uvula and lateral pharyngeal wall, fullness in base of It requires the patient to spend a night.
tongue, lingual tonsillar hypertrophy, banding of posterior Parameters: This highly sensitive and specific test measures
pharyngeal wall, narrow skeletal arch
following elements:
• Laryngopharynx: Lateral pharyngeal wall collapse, omega- Electroencephalogram (EEG) shows brain activity
shaped epiglottis, tumor Electromyogram (EMG) shows chin and leg muscle
• Larynx: Vocal cord palsy and tumor (anterior tibialis) movements
Electrocardiogram (ECG) shows cardiac rhythm
• Neck: Full and thick neck (Pickwickian syndrome) Electrooculogram (EOG) shows eye movements
Pulse oximetry shows blood oxygen saturation
• Children: Tonsil and adenoid hypertrophy, nasopharyngeal Respiratory effort monitoring of chest and abdomen
cyst, encephalocele, choanal atresia, deviated nasal septum Air movement at nose and mouth
and craniofacial or orthodontic malformations Monitoring of body positions
Optional: End-tidal CO2 monitor, esophageal manom-
• General: Obesity, achondroplasia, chest wall deformity,
Marfan’s syndrome. eter, nasal CPAP/bilevel positive airway pressure.
Indications: Not everyone who snores need sleep study.
The snorers, who have following elements, need sleep
study.
Hypersomnolence, morning headache and restless
sleep
Socially disruptive loud snoring
Prior to any surgery for sleep apnea or snoring.
Fig. 1: Kissing tonsils Home Sleep Studies
These measures are economical. They are not as sensitive or
Systemic examination: Further examination is needed in specific as a formal sleep lab polysomnography. Some studies
patients with cor pulmonale or hypertension. measure only pulse oximetry while others have multichannel
recording devices.
Flexible Nasopharyngolaryngoscopy
This endoscopy examination offers a view of entire naso- Multiple Sleep Latency Test
pharynx, laryngopharynx and larynx. This test is done during the day in a sleep laboratory. The patient
Muller’s maneuver: This test is done before the uvulopala- is allowed to take several naps. This test measures the time
that patient takes to fall asleep. An average sleep onset of less
topharyngoplasty (UPPP) to know whether the patient will than 5 minutes indicates excessive daytime sleepiness, which
benefit from this surgery or not. After passing the scope is considered pathologic.
and during the examination, examiner pinches the patient’s
nostrils and patient attempts to inhale with closed mouth. Severity of osa
If the laryngopharynx and/or larynx collapse, it means test Respiratory disturbance index: Respiratory disturbance
is positive. It indicates that obstruction is below the level of
soft palate. These patients will not benefit from UPPP and index (RDI) is the sum of apneas (cessation of breathing/
may need tracheostomy. air flow for > 10 sec) and hypopneas (decrease in air flow
by 50%). On the basis of RDI, OSA can be classified into
Radiography three groups:
Imaging studies may involve lateral cephalometric X-rays, Mild (10–30)
fluoroscopy, CT scan, or MRI. Moderate (30–50)
Standard lateral cephalometric tracings identifies soft-tissue Severe (>50)
Degree of oxyhemoglobin desaturation (SaO2): It is less than
85% in moderate OSA and less than 60% in severe OSA.
Epworth Sleepiness Scale: It assesses the daytime sleepiness
(Table 1). Patients answer the questions on the scale from
0 to 3.
Table 1 Epworth Sleepiness Scale Angina and myocardial infarction 433
Congestive heart failure
Answer the chances of dozing/sleeping in the following Cor pulmonale and chronic heart failure
situations on the scale 0 to 3* Hypertension: Systemic and pulmonary
Peripheral edema
Situation Score* Polycythemia
Excessive day time somnolence can result in
Reading
Accidents during driving vehicle or operating dangerous
Watching TV machines.
Theater/meeting place Less exercise and more weight gain and more severe
sleep apnea.
At traffic light while driving vehicle
Nonsurgical Treatment
Sitting in passenger seat of a car for 1 hour Figure 2 shows the Flow Chart of management of snoring
both with and without OSA. Discomfort and poor compliance
Rest after lunch without alcohol are major stumbling blocks in the nonsurgical measures in Chapter 40 w Sleep apnea and Sleep-disordered Breathing
managing snoring and OSA.
On lying down to rest
Lifestyle Modifications
**Total Score Behavioral modifications (Box 4) though may reduce snoring
and OSA especially in mild cases, patients’compliance is usually
*Score/scale: 0, never doze; 1, slight chance of dozing; 2, a problem.
Moderate chance of dozing; 3, High chance of dozing. Positional therapy: The patient is advised to sleep sideway rather
than on the back. A rubber ball tied to the back of pajama
**Total score less than 8 is normal. prevents the patient to adopt supine position, which aggravates
the symptoms.
Complications of osa
The chronic OSA patients if not treated can develop significant
morbidity and mortality due to following conditions, which can
be reversed to normal with the successful treatment of OSA. The
decrease psychomotor vigilance results in seven fold increase in
the risk of motor vehicle accidents.
Cardiac arrhythmias
Cerebrovascular accidents
Fig. 2: Flow chart of management of snoring both with and without OSA
434 Box 4: Lifestyle modifications for the management of snoring Table 2 Surgical procedures for the treatment of
and OSA OSA
• Adopt an athletic lifestyle and exercise daily Site of Surgical procedures
• Lose weight obstruction
• Avoid sedatives (tranquilizers, sleeping pills, antihistaminics
Nose and Septoplasty, turbinectomy, adenoidectomy,
and cough suppressants) at bed time nasopharynx nasal valve reconstruction, removal of polyps
• Avoid alcoholic drinks within 4 hours of retiring to bed and tumors
• Avoid heavy dinner within 3 hours of going to bed
• Avoid getting overtired Palate Uvulopalatopharyngoplasty (UPPP),
• Establish regular sleeping patterns and tonsil uvulopalatal flap, transpalatal advancement
• Sleep sideway rather than on the back pharyngoplasty, uvulopalatoplasty [Laser-
• Raise the head end of the bed about 4” by placing bricks assisted uvulopalatoplasty (LAUP) or Bovie-
assisted uvulopalatoplasty (BAUP)], palatal
under the bedposts radiofrequency and tonsillectomy
• Nonsnorer partner should go to sleep first.
Tongue Partial glossectomy, lingual tonsillectomy,
Nasal Continuous Positive Airway Pressure tongue base radiofrequency and repose
Section 5 w Pharynx and Esophagus This ventilator type machine is the most effective mean in tongue suspension, hyoid myotomy and
the nonsurgical management of OSA. Continuous positive suspension
airway pressure (CPAP) provides a sort of pneumatic splint to
airway and increases its caliber. Though it is 100% effective in Jaws Maxillomandibular osteotomy and
treating OSA, patient’s compliance is not very good and about advancement, mandibular osteotomy with
30% patients eventually stop using this. In this nasal CPAP, an genioglossus advancement
airtight mask is kept over the patient’s nose with the help of
a strap wrapped around the head. The optimum pressure for Therefore patient should be told that additional procedures
opening the airway, which is determined during sleep study, may be required if UPPP fails.
is usually kept at 5–20 cm of H2O. Complications: They are similar to tonsillectomy and
Bilevel positive airway pressure and Auto-titrating PAP: They includes bleeding (most common), temporary velopharyn-
geal incompetence (in 5–10% of patients) and nasopharyn-
have little better patient compliance. Bilevel positive airway geal stenosis (rare). Other minor postoperative complaints,
pressure (BiPAP) delivers positive pressure at two fixed which are temporary, include dry mouth, throat tightness,
levels—a higher inspiratory and a lower expiratory pressure. increased gag reflex and alteration in taste.
Auto-titrating PAP (APAP) continuously adjusts the pressure.
Other Surgical Procedures
Intraoral Devices Hypopharyngeal and base of tongue procedures: The find-
Tongue-retaining device (TRD) and mandible advancement
ings, which suggest hypopharyngeal obstruction, include
device (MAD) hold the tongue and/or mandible forward Morbid obesity: Body mass index greater than 31 kg/m2
during the sleep and keep the airway open. Similar to CPAP Mandibular skeletal deficiency
discomfort and poor compliance are major concerns. Lateral cephalometric radiogram: PAS less than 11 mm
Flexible laryngoscopy: Narrow retrolingual space
Surgical Treatment of osa
The surgeries are planned according to the location of the –– Muller’s maneuver: Lateral pharyngeal wall collapse
obstruction (Table 2). Apnea-hypopnea index: greater than 30
The following procedures for advancing base of tongue can be
Uvulopalatopharyngoplasty performed in presence of fullness in the base of the tongue.
This technically easy operation is the most common surgery Partial midline glossectomy: This can be performed with
performed for OSA. The oropharyngeal airway is enlarged
in an anterior-superior and lateral dimensions. It is a type the help of either a laser or Bovie cautery.
of radical tonsillectomy. The tonsils and uvula are removed Tongue base radiofrequency: Radiofrequency (RF)
along with the posterior edge of the soft palate. The anterior
and posterior faucial pillars are sutured together. Similarly, needle is inserted submucosally which coagulates tissue
the nasal and oral side mucosas of the cut edge of soft palate and causes scarring. RF can be used in five to six sittings
are sutured together. Patients usually stay for 1 or 2 days in to reduce the size of tongue.
the hospital. Advancement genioplasty with hyoid suspension: In
Results: UPPP is very effective in treating snoring but cases of obstruction at the level of base of tongue,
retrognathia and micrognathia, the airway is enlarged
significant improvement (50% or more reduction in RDI) by advancing genial tubercle of mandible (origin of
in OSA occurs in about 50% of patients. UPPP alone does genioglossus muscle) anteriorly and suspending hyoid
not reduce the mortality of OSA. The tracheostomy and bone from mandible by permanent sutures or wire. A
CPAP have shown dramatic improvement in OSA mortality. rectangular chin portion of mandible including genial
tubercles is resected and then rotated 90° and fixed
by plates.
Hyoid myotomy and suspension:The midline hyoid bone
is isolated and then advanced over thyroid cartilage.
Mandibular and maxillary advancement: This procedures is Surgical Treatment of Snoring 435
more major than UPPP. It employs sagittal split and LeFort without OSA
I osteotomies. These osteotomies are then fixed in anterior Chapter 40 w Sleep apnea and Sleep-disordered Breathing
position with plates and screws. They effectively treat the Uvulopalatoplasty: Laser-assisted uvulopalatoplasty
anatomic anomalies causing OSA and offer long-lasting (LAUP) or Bovie-assisted uvulopalatoplasty (BAUP)
results. can be performed under local anesthesia as an OPD
procedure. In this procedure uvula is amputated and
Nasal surgery: Though rarely a sole cause, nasal obstruction 1 cm trenches are created in the soft palate on either side of
should be managed according to its cause and procedures the uvula. The soft palate elevates and stiffens after healing.
include septoplasty, septal surgery and removal of polyps It may be performed in two to four stages, each separated by
and tumors. about 1 month. In this way the soft palate resection is titrated
to treat snoring without velopharyngeal incompetence.
Tracheostomy: Though neither preferred by surgeon nor It is highly effective and resolution of snoring occurs in
liked by the patient this gold standard treatment of OSA is 85–90% of patients. Though it may help in mild or moderate
almost 100% effective. Tracheostomy bypasses the upper OSA, generally it is contraindicated in cases of OSA.
airway entirely but needs daily care throughout the life,
which is a major stumbling block. It is probably the first UPPP is also very effective in treating snoring.
line of surgery in very severe OSA or in those who are
significantly obese or debilitated.
Clinical Highlights
1. Causes of snoring: Some of the causes of snoring are nasopharyngeal angiofibroma, tonsillar enlargement, antrochoanal
polyp and adenoid hypertrophy.
2. Muller’s maneuver: It is performed with flexible nasopharyngolaryngoscopy to find the level and degree of obstruction
in cases of obstructive sleep apnea. The patient is requested to make maximal inspiratory effort with nose and mouth
closed. The base of tongue, lateral pharyngeal wall and palate are examined for collapsibility. The severity is rated from
0 (minimal collapse) to 4+ (complete collapse).
FURTHER READING
1. Bhawna, Santosham R, Anand S, et al. Role of dynamic MR imaging in obstructive sleep apnoea. Indian J Otolaryngol Head Neck Surg.
2008;60:25-9.
2. Rao JJ, Kumar VEC, Chowdary SV, et al. CT-cephalometry-A study in Indian population. Indian J Otolaryngol Head Neck Surg. 2005;57:30-4.
3. Safaya A. Snoring-A mesopharyngometric profile. Indian J Otolaryngol Head Neck Surg. 2001;53:36-40.
4. Safaya A, Suri JC, Batra K. Uvulopalatopharyngoplasty-Surgery for snoring. Indian J Otolaryngol Head Neck Surg. 2002;54:204-7.
5. Vinaya Kumar EC, Rao J, Chowdhay S, et al. Management of tongue base obstruction in obstructive sleep apnoea syndrome. Indian J
Otolaryngol Head Neck Surg. 2000;52:58-62.
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